Coronavirus Updates January 2024

[missy]

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The 2024 Adult Vaccine Schedule Changes Are Here​

Publish date: December 27, 2023
By
Sandra Adamson Fryhofer, MD

This transcript has been edited for clarity.
Sandra Fryhofer, MD, highlights updates in the 2024 Advisory Committee on Immunization Practices (ACIP) Adult Immunization Schedule.
The biggest change for 2024 is that you don’t need to wait till January 1, 2024, for these schedules go into effect. Both schedules were published and became available in November 2023 and became effective immediately. They include ACIP recommendations approved by the Centers for Disease Control and Prevention (CDC) director through October 23, 2023.

Subsequent recommendations (before publication of the 2025 schedule) will be added to the addendum, a new Step 5, Section 5 in the schedule. The addendum should make Affordable Care Act (ACA)–compliant insurance plans cover ACIP-recommended immunizations sooner.
This year’s schedule includes more vaccines with new recommendations and new color code keys for the schedule’s vaccine tables. The newest vaccine additions to the 2024 schedule include respiratory syncytial virus (RSV) vaccines, the mpox vaccine (Jynneos), a new MenACWY-MenB combo vaccine (Penbraya), and the new 2023-2024 formulation of the updated COVID vaccine (both mRNA and protein-based adjuvanted versions).
These are listed on the cover page (in alphabetical order) by name, abbreviation, and trade name. Vaccine-specific details can be found in the (Step 3) Notes section, also organized alphabetically.

The Tables​

Step 1 is Table 1: Vaccinations by Age. Step 2 is Table 2: Vaccinations by Medical Conditions or Other Indications. The table names haven’t changed. However, their color code legends have been adjusted and refined. Also, the legends for the some of the same colors are not the same for both tables.
The order of and conditions covered in the columns on Table 2 have been reorganized.
Even for vaccines whose recommendations have not changed, the color code keys reflecting the recommendations have changed. For this reason, the 2024 version of Table 2 looks very different from the 2023 version. Also, much of the wording on overlays has been removed, which means you have to rely more heavily on the Notes section.
The color brown has been introduced on Table 2 to spotlight groups and conditions that require recurrent revaccination:

• Give Tdap in each and every pregnancy at 27-36 weeks.
• Revaccinate people living with HIV with MenACWY every 5 years.
• Revaccinate those with asplenia and/or complement deficiency with MenACWY every 5 years and MenB every 2-3 years.
• Stem cell transplant recipients need three doses of Hib.

Vaccine order is the same on both tables.
The rows for 2023-2024 formulations of COVID and flu vaccines are at the top of both tables are coded yellow, meaning everyone needs a dose of both vaccines.
Both tables have added a row for RSV vaccines and mpox vaccines.

Notes Section​

The notes have been edited for clarity and reveal who needs what and when and include special vaccine-specific sections for special circumstances.
COVID vaccines. The COVID vaccine note embraces the updated 2023-2024 formula. Everyone aged 6 months or older needs a dose of the updated COVID vaccine. Specifics of who needs what (and when) depend on what they have already received, as well as their immune status. Detailed recommendations for both mRNA and protein-based adjuvanted versions are included in the notes.
RSV vaccines. The notes also give vital details about RSV vaccines for pregnant people and for older adults. There are two RSV vaccines. Both are preF RSV vaccines. They’re identified by trade names for clarity. Arexvy contains an adjuvant. Abrysvo does not contain an adjuvant. The RSV vaccine note explains that only Abyrsvo (the vaccine without the adjuvant) can be given to pregnant people, only at 32-36 weeks, and only to those whose baby would be born during RSV season.
ACIP recommends a dose of either vaccine for adults aged 60 or older, under shared clinical decision-making (meaning you and your patients have to discuss and decide). The notes link to additional guidance for making that decision.
Mpox vaccines. For the mpox vaccine, all adults in any age group at increased risk of getting mpox should get a two-dose series of the vaccine. The mpox vaccine notes include a list of mpox risk factors.

Other Features of the 2024 Adult Immunization Schedule​

The schedule has useful links to helpful information:

• Vaccine information statements
• Complete ACIP recommendations
• CDC’s General Best Practice Guidelines for Immunizations.
• VAERS (CDC’s Vaccine Adverse Event Reporting System)

A new “Additional Information” section in the Notes links to:

• Travel vaccination requirements
• Best practices guidelines for vaccinating persons with immunodeficiency
• The National Vaccine Injury Compensation program (for resolving any vaccine injury claims)

The cover page has links to:

• CDC’s vaccine app
• QR code to access the schedule online.

With all these tools literally at your fingertips, there’s no reason not to know which vaccines your patients need and when. The challenge now is making it happen: getting those needed vaccines into arms.
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[missy]

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FROM THE JOURNALS

Monoclonal Antibodies: A New Treatment for Long COVID?​

FROM THE AMERICAN JOURNAL OF EMERGENCY MEDICINe
A treatment used to treat acute COVID-19 infection has also been found to be effective against long COVID, a new small study has found. The research, which assessed the benefits of monoclonal antibodies, suggests relief may finally be ahead for millions of Americans with long COVID for whom treatment has remained elusive.
The study, published in the American Journal of Emergency Medicine, found three Florida patients with long COVID made complete — and sudden — recoveries after they were given the monoclonal antibody cocktail casirivimab/imdevimab (Regeneron).
“We were struck by how rapid and complete the remissions were,” said study coauthor Paul Pepe, MD, MPH, a professor of management, policy, and community health at the School of Public Health at the University of Texas Health Sciences Center. “We found that no matter how long the patients were sick for — whether it was 5, 8, or 18 months — within 5 days, they appeared to be completely cured.”

All three patients had been initially infected with COVID-19 early in the pandemic, in 2020 or the first half of 2021. They were given Regeneron either after a reinfection or exposure to COVID-19, as a preventative, at state-run COVID clinics in Florida.
“In each case, the infusions were given to help prevent their long COVID from worsening,” said Dr. Pepe.
The researchers collected medical histories for all three patients, asking about symptoms such as physical fatigue, exercise intolerance, chest pain, heart palpitations, shortness of breath, cognitive fatigue, and memory problems. They asked patients to rate symptoms pre-COVID (baseline), during the long COVID phase, post-vaccine, and finally a week after their monoclonal antibody treatment. They also interviewed family members.
They found that across the board, symptoms improved significantly and often completely vanished. Their loved ones corroborated these reports as well.
One of the patients, a 63-year-old Floridian woman, came down with a mild case of COVID-19 at the start of the pandemic in March 2020 that lasted about 2 weeks. But several weeks later, she developed extreme, debilitating fatigue, along with chest pain and shortness of breath.
“I was chasing my 6-pound Yorkie one day after she got loose, and I was struck with such intense chest pain I fell down,” the woman, asking not to be identified, said in an interview.
Her symptoms progressed to the point where she no longer felt safe babysitting her grandchildren or driving to the grocery store.
“My short-term memory was completely gone. I couldn’t even read more than a paragraph at a time,” she said.
When she was exposed to COVID-19 in October 2021, her doctor suggested Regeneron as a preventative. She agreed to it.
“I was terrified that a second round would leave me permanently disabled and stuck in bed for the rest of my life,” she said.
About 4 days after her monoclonal antibody treatment, she noticed that some of the brain fog that had persisted after COVID was lifting.
“By day 5, it felt almost like a heavy-weighted blanket had been lifted off of me,” she recalled. “I was able to take my dog for a walk and go to the grocery store. It felt like I had gone from 0 to 100. As quickly as I went downhill, I quickly went back up.”
FROM THE AMERICAN JOURNAL OF EMERGENCY MEDICINe

Reasons for Recovery​

Researchers have come up with a few theories about why monoclonal antibodies may help treat long COVID, said study coauthor Aileen Marty, MD, professor of translational medicine at the Herbert Wertheim College of Medicine at Florida International University. Among them:

• It stimulates the body to fight off any residual virus. “We suspect that many of these patients simply have levels of virus that are so low they can’t be picked up by conventional testing,” said Dr. Marty. “The virus lingers in their body and causes long COVID symptoms. The monoclonal antibodies can zero in on them and knock them out.” This may also help explain why some patients with long COVID reported a temporary improvement of symptoms after their COVID-19 vaccination.
• It combats dysfunctional antibodies. Another theory is that people with long COVID have symptoms “not because of residual virus but because of junky antibodies,” said Dr. Marty. These antibodies go into overdrive and attack your own cells, which is what causes long COVID symptoms. “This may be why monoclonal antibodies work because they displace the dysfunctional antibodies that are attached to a patient’s cells,” she explained.
• Reactivation of other viruses. Long COVID is very similar to chronic fatigue syndrome, which is often thought to be triggered by reactivation of viruses like the Epstein-Barr virus, noted coauthor Nancy Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Fort Lauderdale. “It may not explain all of the cases of long COVID, but it could make up a subgroup,” she said. It’s thought that the monoclonal antibodies may perhaps neutralize this reactivation.

Where Research Is Headed​

While Regeneron worked well in all three patients, it may be because they developed long COVID from either the initial virus or from early variants like Alpha, Beta, and Delta, said Dr. Pepe. As a result, it’s unclear whether this treatment would work for patients who developed long COVID from newer strains like Omicron.
“What concerns me is I believe there may be many people walking around with mild long COVID from these strains who don’t realize it,” he said. “They may assume that if they have difficulty walking upstairs, or forget why they went into another room, that it’s age related.”

The next step, the researchers said, is to create a registry of volunteer patients with severe long COVID. Dr. Klimas plans to enroll 20 volunteers who were infected before September 2022 to see how they respond to another monoclonal antibody initially used to treat COVID-19, bebtelovimab. (Like Regeneron, bebtelovimab is no longer approved for use against COVID-19 by the US Food and Drug Administration because it is no longer effective against variants of the virus circulating today.)
As for patients who developed long COVID after September 2022, research is ongoing to see if they respond to other monoclonal antibodies that are in development. One such study is currently enrolling participants at the University of California San Francisco. The center is recruiting 30 patients with long COVID to try a monoclonal antibody developed by Aerium Therapeutics.
“They created an investigational monoclonal antibody to treat acute COVID, but it proved less effective against variants that emerged in late 2022,” said lead investigator Michael Peluso, MD, an assistant professor of medicine in the Division of HIV, Infectious Diseases, and Global Medicine at the University of California San Francisco. The hope is it may still work to fight long COVID among patients infected with those variants.
In the meantime, the three patients with long COVID who responded to Regeneron have resumed life as they knew it pre-COVID. Although two subsequently became infected with COVID again, they recovered quickly and did not see symptoms return, something which, for them, seems nothing short of miraculous.
“I had prepared myself to be disabled for life,” said one of the patients, a 46-year-old Floridian woman who developed long COVID after an infection in January 2021. “I had crippling fatigue and dizziness so intense I felt like I was walking on a trampoline. My brain fog was so pronounced I had to write everything down constantly. Otherwise, I’d forget.”
When she became infected with COVID again in September 2021, “I thought I was going to die because I had no idea how I could possibly get worse,” she recalled. Her doctors recommended Regeneron infusion treatment. Forty-eight hours later, her symptoms improved significantly.
“I was able to go out to a cocktail party and dinner for the first time in months,” she said. “I would not have been able to do either of those things a week before.”
It’s also profoundly affected her husband, who had had to take over running the household and raising their five children, aged 11-22 years, for months.
“I can’t tell you how many school events and sports games I missed because I physically didn’t have the strength to get to them,” she noted. “To this day, my husband gets upset whenever we talk about that time. Long COVID literally took over all of our lives. It was devastating to me, but it’s just as devastating for loved ones, too. My family is just grateful to have me back.”

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[missy]

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ME/CFS and Long COVID: Research Aims to Identify Treatable, Druggable Pathways​

Publish date: January 2, 2024
By
Miriam E. Tucker

FROM AN NIH RESEARCH CONFERENCE
BETHESDA, MD — New research into the mechanisms underlying myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID is aimed at identifying potential approaches to treatment of the two overlapping illnesses.
According to a new data brief from the National Center for Health Statistics, in 2021-2022, 1.3% of US adults had ME/CFS, a complex, multisystem illness characterizedby activity-limiting fatigue, worsening of symptoms after exertion, unrefreshing sleep, and other symptoms.
A 2-day conference, Advancing ME/CFS Research: Identifying Targets for Potential Intervention and Learning from Long COVID, was held in December 12-13 on the main campus of the US National Institutes of Health (NIH) and was livestreamed. The last such meeting, also featuring results from NIH-funded research, was held in April 2019.

“Things have changed since 2019 ... The idea of this meeting is to try and identify pathways that will be treatable and druggable and really make an impact for patients based on the things that we’ve learned over the last number of years and including, fortunately or unfortunately, the huge number of people who are suffering from long COVID, where the symptoms overlap so much with those who have been suffering for a long time with ME/CFS,” said Conference Chair Joe Breen, PhD, of the National Institute of Allergy and Infectious Diseases.
As in 2019, the meeting was preceded by a day of research presentations from young investigators, some of whom also presented their findings at the main meeting. New this year were four “lived experience” speakers who described their physical, emotional, and financial struggles with ME/CFS or long COVID. Two of them presented virtually because they were too ill to travel.
Social worker and patient advocate Terri Wilder of Minneapolis, Minnesota, reported some feedback she received on social media after she asked people with ME/CFS about their priorities for the research and clinical communities.
Among the top responses were the need to recognize and study the phenomenon of “post-exertional malaise” and to stop recommending exercise for people with these illnesses, to accelerate research to find effective treatments, and to put an end to stigma around the condition. “People don’t believe us when we tell them we’re sick, people make fun of us, misperceptions persist,” Wilder said.
One person commented, “[Clinicians] shouldn’t be afraid to try off-label meds with us if needed. There may be some secondary effects, but they are better options than us taking our own lives because we can’t stand the suffering.”
Research areas covered at the conference included immunology, virology, metabolism, gene regulation, and neurology of both ME/CFS and long COVID, as well as the latest findings regarding the overlap between the two conditions.

Oxidative Stress in Both ME/CFS and Long COVID: A Role for Metformin?​

Mark M. Davis, PhD, professor and director of the Institute for Immunity, Transplantation, and Infection at Stanford University, Palo Alto, California, summarized published data suggesting that oxidative stress is a shared characteristic of both ME/CFS and long COVID. Most cellular reactive oxygen species (ROS) are produced in the cell’s mitochondria, and T-cell activation is ROS-dependent.
Women in particular with ME/CFS show high ROS levels with consistent T-cell hyperproliferation, “which can be suppressed with specific drugs such as metformin. This raises the prospect of optimizing drug treatment and drug discovery with a simple in vitro assay of the effects on a patient’s lymphocytes,” Dr. Davis said. He also cited a study suggesting that metformin may help prevent long COVID.
Asked to comment on that, longtime ME/CFS researcher Anthony L. Komaroff, MD, of Harvard University, Cambridge, Massachusetts, cautioned that although metformin is used safely by millions of people with type 2 diabetes worldwide, it’s possible that some people with ME/CFS may be more likely to experience its known adverse effects such as lactic acidosis.
To repurpose metformin or any other already-marketed drugs for ME/CFS and/or long COVID, Dr. Komaroff said, “We should entertain treatment trials.” However, as he and many others lamented at the conference, funding for off-patent drugs often isn’t forthcoming.

Addressing the Microbiome, Innate Immunity​

W. Ian Lipkin, MD, of Columbia University, New York, NY, was one of two speakers who discussed the role of disruptions in the microbiome and innate immunity in ME/CFS. He presented data suggesting that “dysregulation of the gut microbiome in ME/CFS may interfere with butyrate production, resulting in inflammation and porosity to bacteria and bacterial products that trigger innate immunity.”
Dr. Lipkin highlighted a “really intriguing” paper in which exogenous administration of interleukin 37 (IL-37), a naturally occurring inhibitor of inflammation, reversed the decrease in exercise performance observed during inflammation-induced fatigue and increased exercise performance, both in mice.
“Although we do not fully understand the pathophysiology of ME/CFS, it is not premature to consider randomized clinical trials of pro- and pre-biotics that address dysbiosis as well as drugs that modify innate immune responses such as poly (I:C)and IL-37,” Dr. Lipkin said.

Alleviating Endoplasmic Reticulum (ER) Stress: A Strategy to Increase Energy?​

Paul M. Hwang, MD, PhD, from the Cardiovascular Branch of the National Heart, Lung, and Blood Institute, Bethesda, Maryland, described work that he and his colleagues recently published around a case of a 38-year-old woman with Li-Fraumeni syndrome, a genetic early-onset cancer, who also had extensive fatigue, exercise intolerance, and post-exertional malaise that began after she contracted mononucleosis as a teenager.
Testing revealed that her cells had increased expression of Wiskott-Aldrich Syndrome Protein Family Member 3 (WASF3), a “top candidate” gene found to be associated with ME/CFS in a bioinformatics study published more than a decade ago. Moreover, immunoblotting of deidentified skeletal muscle biopsy samples obtained from patients with postinfectious ME/CFS also revealed significantly increased WASF3 levels.
Hwang and colleagues showed in mice that ER stress–induced WASF3 protein localizes to mitochondria and disrupts respiratory supercomplex assembly, leading to decreased oxygen consumption and exercise endurance.
However, use of the investigational protein phosphatase 1 inhibitor salubrinal in the female patient’s cells inhibited the ER stress, which in turn decreased WASF3 expression and improved mitochondrial supercomplex formation and respiration, “suggesting a treatment strategy in ME/CFS,” Dr. Hwang said.

Neurovascular Dysregulation During Exercise: A Role for Pyridostigmine?​

David M. Systrom, MD, a pulmonary and critical care medicine specialist at the Brigham and Women’s Hospital, Boston, Massachusetts, gave an update of his work investigating neurovascular dysregulation during exercise in both ME/CFS and long COVID using invasive cardiopulmonary testing.
In a 2021 publication, Dr. Systrom and his colleagues identified the mechanism of “preload failure,” or lower filling pressures of blood in the heart chambers because of insufficient vein constriction and reduced return of blood to the right side of the heart in people with ME/CFS, compared with healthy controls.
Subsequently, in a randomized trial of 45 patients with ME/CFS, Systrom and his colleagues published in November 2022, use of the cholinesterase inhibitor pyridostigmine, currently approved for treating myasthenia gravis and related conditions, improved peak Vo2 by increasing cardiac output and filling pressures.
Now, Dr. Systrom’s team is conducting a randomized trial comparing 60 mg pyridostigmine with or without low-dose naltrexone (LDN) vs placebo in 160 patients with ME/CFS for 3 months. Metabolomic, transcriptomic, proteomic, and other assessments will be conducted on urine and blood samples. Participants will also wear devices that measure steps, sleep, heart rate, and other metrics.
Komaroff cautioned that pyridostigmine, too, has potential adverse effects. “I’m not sure pyridostigmine is ready for prime time ... It’s a drug developed for a very different purpose ... Now will it hold up in a larger trial, and will there be any side effects that turn up in larger studies? It’s not unreasonable to study.”

Brain Inflammation: Measuring and Treating It​

Hannah F. Bues, clinical research coordinator at Massachusetts General Hospital, Boston, presented data now in preprint (ie, not yet peer-reviewed) in which researchers used [11C]PBR28 PET neuroimaging, a marker of neuroinflammation, to compare 12 individuals with long COVID vs 43 healthy controls. They found significantly increased neuroinflammation in several different brain regions in the long COVID group compared with controls.
Samples of peripheral blood plasma also showed significant correlations between neuroinflammation and circulating analytes related to vascular dysfunction. This work is ongoing in both long COVID and pre-COVID ME/CFS populations, Bues said.
Jarred Younger, PhD, of the Neuroinflammation, Pain, and Fatigue Laboratory at the University of Alabama, Birmingham, also gave an update of his ongoing work demonstrating significant brain inflammation seen in neuroimaging of people with ME/CFS compared with healthy controls.

Dr. Younger has been investigating the use of LDN for pain in fibromyalgia. Anecdotally, there have been reports of fatigue reduction with LDN in ME/CFS.
Dr. Younger conducted a post hoc analysis of his previous trial of LDN for 12 weeks in 30 patients with fibromyalgia. Of those, 16 met older CFS criteria. There was a significant reduction in their fatigue severity, with P <.0001 from baseline and P < .009 compared with placebo. The P values were high because the data included daily symptom reports. The average fatigue reduction was 25%.
“It wasn’t a study designed for ME/CFS, but I think it’s compelling evidence and enough with the other types of data we have to say we need to do a proper clinical trial of low-dose naltrexone in ME/CFS now,” Dr. Younger said.

‘We Need to Do Something’ About the Underfunding​

Another NIH-funded ME/CFS researcher, Maureen Hanson, PhD, of Cornell University, Ithaca, NY, noted that the NIH currently funds ME/CFS research at about $13 million compared with $1.15 billion for the Researching COVID to Enhance Recovery Initiative granted to NIH by Congress for “post-acute sequelae of SARS-CoV-2 (PASC)” in 2021 “because of the urgency of studying this. Most of us here are well aware of the underfunding of ME/CFS relative to the burden of illness,” she said.
Current 2024 funding for AIDS research is $3294 million. “There are 1.2 million individuals living with HIV in the United States, and there are over 3 million who are barely living with ME/CFS in the United States. We need to do something about this ... It’s certainly possible that future funding for PASC is now going to disappear,” Dr. Hanson cautioned.
Wilder, the patient advocate, reminded the audience that “There is a cohort of people with ME who got sick in the 1980s and 1990s in the prime of their life ... They have dreamed of a day when there would be a major announcement that a treatment has been discovered to take away the suffering of this disease ... They keep waiting and waiting, year after year, missing more and more of their lives with each passing day ... We’re all depending on you.”
Dr. Systrom has received funding from the Solve ME/CFS Initiative, Department of Defense, and Open Medicine Foundation. Dr. Younger’s work is funded by the NIH, Department of Defense, SolveME, the American Fibromyalgia Association, and ME Research UK. Dr. Lipkin and Dr. Hanson receive NIH funding. Dr. Komaroff has no disclosures.
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[dk168]

Covid is still alive and kicking and I know of a few people who have got it recently.

Personally, I would perform LFT if I start to get flu like symptoms, and have a supply of LFTs at home.

If tested positive, I would self-isolated for 5 days at least, which was what I did back in July 2023 when I got Covid after returning from a work related trip from the Netherlands.

DK

 

[missy]

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Long COVID Has Caused Thousands of US Deaths: New CDC Data​

Lisa Rapaport
January 03, 2024

While COVID has now claimed more than 1 million lives in the United States alone, these aren't the only fatalities caused at least in part by the virus. A small but growing number of Americans are surviving acute infections only to succumb months later to the lingering health problems caused by long COVID.
Much of the attention on long COVID has centered on the sometimes debilitating symptoms that strike people with the condition, with no formal diagnostic tests or standard treatments available, and the effect it has on quality of life. But new figures from the US Centers for Disease Control and Prevention (CDC) show that long COVID can also be deadly.
More than 5000 Americans have died from long COVID since the start of the pandemic, according to new estimates from the CDC.

This total, based on death certificate data collected by the CDC, includes a preliminary tally of 1491 long COVID deaths in 2023 in addition to 3544 fatalities previously reported from January 2020 through June 2022.
Guidance issued in 2023 on how to formally report long COVID as a cause of death on death certificates should help get a more accurate count of these fatalities going forward, said Robert Anderson, PhD, chief mortality statistician for the CDC.
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"We hope that the guidance will help cause of death certifiers be more aware of the impact of long COVID and more likely to report long COVID as a cause of death when appropriate," Anderson said. "That said, we do not expect that this guidance will have a dramatic impact on the trend."

There's no standard definition or diagnostic test for long COVID. It's typically diagnosed when people have symptoms at least 3 months after an acute infection that weren't present before they got sick. As of the end of last year, about 7% of American adults had experienced long COVID at some point, the CDC estimated in September 2023.
The new death tally indicates long COVID remains a significant public health threat and is likely to grow in the years ahead, even though the pandemic may no longer be considered a global health crisis, experts said.
For example, the death certificate figures indicate:

• COVID-19 was the third leading cause of American deaths in 2020 and 2021, and the fourth leading cause of death in the United States in 2023.
• Nearly 1% of the more than one million deaths related to COVID-19 since the start of the pandemic have been attributed to long COVID, according to data released by the CDC.
• The proportion of COVID-related deaths from long COVID peaked in June 2021 at 1.2% and again in April 2022 at 3.8%, according to the CDC. Both of these peaks coincided with periods of declining fatalities from acute infections.

"I do expect that deaths associated with long COVID will make up an increasingly larger proportion of total deaths associated with COVID-19," said Mark Czeisler, PhD, a researcher at Harvard Medical School who has studied long COVID fatalities.
Months and even years after an acute infection, long COVID can contribute to serious and potentially life-threatening conditions that impact nearly every major system in the body, according to the CDC guidelines for identifying the condition on death certificates.
This means long COVID may often be listed as an underlying cause of death when people with this condition die of issues related to their heart, lungs, brain or kidneys, the CDC guidelines noted.
The risk for long COVID fatalities remains elevated for at least 6 months for people with milder acute infections and for at least 2 years in severe cases that require hospitalization, some previous research suggested.
As happens with other acute infections, certain people are more at risk for fatal case of long COVID. Age, race, and ethnicity have all been cited as risk factors by researchers who have been tracking the condition since the start of the pandemic.
Half of long COVID fatalities from July 2021 to June 2022 occurred in people aged 65 years and older, and another 23% were recorded among people aged 50-64 years old, according a report from CDC.
Long COVID death rates also varied by race and ethnicity, from a high of 14.1 cases per million among America Indian and Alaskan natives to a low of 1.5 cases per million among Asian people, the CDC found. Death rates per million were 6.7 for White individuals, 6.4 for Black people, and 4.7 for Hispanic people.
The disproportionate share of Black and Hispanic people who developed and died from severe acute infections may have left fewer survivors to develop long COVID, limiting long COVID fatalities among these groups, the CDC report concluded.

It's also possible that long COVID fatalities were undercounted in these populations because they faced challenges accessing healthcare or seeing providers who could recognize the hallmark symptoms of long COVID.
It's also difficult to distinguish between how many deaths related to the virus ultimately occur as a result of long COVID rather than acute infections. That's because it may depend on a variety of factors, including how consistently medical examiners follow the CDC guidelines, said Ziyad Al-Aly, MD, chief of research at the Veterans Affairs, St. Louis Health Care System and a senior clinical epidemiologist at Washington University in St. Louis.
"Long COVID remains massively underdiagnosed, and death in people with long COVID is misattributed to other things," Al-Aly said.

An accurate test for long COVID could help lead to a more accurate count of these fatalities, Czeisler said. Some preliminary research suggests that it might one day be possible to diagnose long COVID with a blood test.
"The timeline for such a test and the extent to which it would be widely applied is uncertain," Czeisler noted, "though that would certainly be a gamechanger."
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[missy]

Hospitals in our area are now requiring masks again FYI

 

[kathley]

Ours are too. Cases are really ramping up with very sick people lining the ER halls.

 

[dk168]

Saw this and thought it is worth sharing, don't shoot the messenger please as I am not certain if it is entirely accurate!




DK

 

[missy]

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Covid-19 research roundup: Jan 11​

KATELYN JETELINA

There are several new scientific developments regarding Covid-19 that might be useful to you, given that we are in a big wave right now. Here is a quick research roundup.

(Note: I will dive deeper into long Covid next week. We’ve learned a lotmore over the past year. Stay tuned.)

Fall 2023 vaccines are effective​

What we know: Recommendations for an updated 2023 Covid-19 vaccine were based on lab and some human data. We didn’t have real-world data or clinical trial efficacy data. (This follows a similar model to the flu.)

New info: Vaccine effectiveness data is rolling in:

• 70% effectiveness against hospitalization (preprint; Netherlands; among 60+ year-olds previously vaccinated).
• Another study found significant added protection for (at least) 30 days against emergency department use, outpatient use, and hospitalization. (Kaiser; among those over 18 years.)

Why does this matter? If you’re up-to-date on vaccines, you can be confident it’s providing additional protection.

Vaccines help protect against long covid​

What we know: Vaccines have many benefits, including preventing long covid. We didn’t know the incremental benefit of additional doses.

New info: A recent study showed that the more vaccines you get, the less likely you will get long covid. This is called a dose-response relationship: One dose of vaccine reduces risk by 21%, 2 doses reduce by 59%, and 3+ doses reduce by 73%.

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Why does it matter? Most people still pay attention to Covid-19 to prevent long covid. Keeping up with vaccines helps a lot.

Children and vaccines​

New info: We’ve been lacking real-world effectiveness data among children lately. The evidence is flooding in now. Four recent studies show:

• Vaccines were highly effective against infection and severe disease across all pandemic periods. Across 4 Nordic countries, for example, there was 73% vaccine effectiveness against severe disease among adolescents. The risk difference was 2 per 10,000 adolescents vaccinated.
• Vaccines are safe. The rate and cause of sudden cardiac death in young people was not due to vaccines during the pandemic. One study even included autopsy investigations.

Transmission takes hours​

New info: Transmission increased linearly by 1% chance per hour. Most transmission resulted from exposures lasting one hour to several days. Households accounted for 6% of contacts but 40% of transmissions.

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Figure from Ferretti et al., 2023.. Nature. Source here.
Why does this matter? Transmission = time x proximity. This may help your risk calculations. Quick passersby at a grocery store are far less risky than staying in a house with someone infected.

JN.1 is more severe?​

New info: Lab data suggests that JN.1 (the dominant subvariant today) is more severe on a microscopic level than other Omicron variants.

Why does this matter? We don’t know whether this has implications on an individual level (i.e., feeling more crappy). But, it does not seem to affect a population level (hospitalizations are less common than last year). Regardless, it may be worth doubling down on protections right now.

Covid-19 viral load peaking later​

What we knew: The virus and our immunity wall have changed significantly over time, which may have implications for antigen testing.

New info: A new study showed that, during the Omicron era, viral load peaked (i.e., had low values in the graph below) on days 3-4. This is very different than the beginning of the pandemic when it peaked at the start of symptoms. (They also looked at the flu, which peaked on days 1-2.)

​

Original image from Frediani et al., 2023; Annotations by YLE
Why does this matter? You may not reliably test positive on a rapid antigen test until the third, fourth, or even fifth day of symptoms. This raises questions on how best to use tests, too, like with Paxlovid (which needs to be given within 5 days of symptoms) and isolation.

No seasonality?​

What we knew: Other viruses are sensitive to temperatures, partially explaining the seasonality patterns of flu and the common cold, for example.

What’s new: A recent animal study suggested SARS-CoV-2 transmission is not driven by temperature or humidity changes. SARS-CoV-2 remains capable of transmission under a variety of temperature and humidity conditions. This is surprising.

Why does this matter? We will likely continue to see multiple waves per year, as human behavior and immune status dominantly determine when we get waves of Covid-19 infection, not the environment.

Bottom line​

Although we are four years into this thing, we still learn every day. Yes, science can still help us make better and more informed decisions.

You’re now caught up.


"

 

[AdaBeta27]

https://www.npr.org/2024/01/13/1224589127/a-discovery-in-the-muscles-of-long-covid-patients-may-explain-exercise-troubles

Mitochondrial Enhancers for Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Pt. I: D-Ribose, CoQ10 and PQQ - Health Rising

This is the first part in a series on mitochondrial enhancers for chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), and long COVID series. The series uses the book “Mitochondria and the Future of Medicine”, by Lee Know, a former naturopathic doctor in Canada, as a starting point, and...

www.healthrising.org

 

[missy]

Breaking Down the Latest on Long COVID Research​

— Ziyad Al-Aly, MD, explains long COVID symptoms, potential causes, and why it's so hard to study​

by Jeremy Faust, MD, MS, MA, Editor-in-Chief, MedPage Today ; Emily Hutto, Associate Video Producer January 19, 2024
Jeremy Faust, MD, editor-in-chief of MedPage Today, and Ziyad Al-Aly, MD, chief of the Research and Education Service at the VA St. Louis Health Care System in Missouri, discuss the latest long COVID research and what it could mean for potential future treatments.

The following is a transcript of their remarks:

"

Faust: My first question is how many different diseases do you think long COVID is? Is it one, is it two, is it five? What do you think?



Al-Aly: Well, long COVID is really a multi-systemic disease. There's no one long COVID; there are likely to be many subtypes.

Our understanding of long COVID now is actually literally embryonic. It's in its infancy. We've made a lot of progress over the past several years, but we need to also recognize that we've only been researching this and understanding long COVID for literally only 4 years.

I tell people when we first started thinking and discovering neoplasm or tumor growth or cancer, we sort of defined, "Oh, this is a lump," or, "This is a cancer" -- and now we have 800 different types of cancer because we understand the biology more. We understand the molecular and genetic fingerprints of cancer much more deeply. We understand tissue-based biology of cancer much more deeply than we did, let's say, 50 years ago. And long COVID is the same thing.



Long COVID is really this post-viral illness or the lingering or enduring problems that happen after SARS CoV-2 infection. We know so far it can affect nearly every organ system. It can affect the heart, the brain, can have metabolic sequela and we're starting to see studies subtyping long COVID into different types.

There are cardinal manifestations that a lot of the audience might have heard of: brain fog, fatigue, post-exertional malaise, or some form of dysautonomia, or postural orthostatic tachycardia syndrome [POTS], or more broadly dystonia or a dysfunction in the autonomic nervous system that would lead to subsequent manifestation. Those are the cardinal manifestations. But really, there is no organ in the body now, 4 years into it, that long COVID does not touch.

Faust: One of the audience questions was whether you see a similarity between long COVID and ME/CFS, myalgic encephalomyelitis/chronic fatigue syndrome. And I'm really interested in this because on one hand I could see it being a good framework to understand these conditions as similar, but also could be a disservice if they're different. What do you think?



Al-Aly: I think there's a lot of overlap.

I mean, ME/CFS itself -- to start with the origin of ME/CFS -- is also thought to be triggered by a viral illness, by a flu-like illness. The onset of ME/CFS doesn't happen in a vacuum. It actually is triggered initially by a viral illness. So, there are likely common etiologic drivers. It may not be the same virus, but it is triggered by a viral illness.

There's a lot of overlap in the symptomatology -- fatigue, brain fog, post-exertional malaise, POTS -- there's quite a bit of overlap in the symptomatology between ME/CFS and long COVID.

It doesn't mean that all the facets are identical. It just means that it sort of gives us hints. The viruses are giving us hints that the viruses we thought initially only caused acute problems or acute disease can in some instances lead to chronic illness or chronic disease. ME/CFS is one example, COVID is another example.



And one of the arguments that I actually find really interesting is that had we as a community of scientists listened to ME/CFS patients a long time ago and really understood it better and [did] more research on it, we'd actually be better and more equipped and more able to address the challenges of long COVID more. We just ignored it. We literally had the Spanish flu pandemic, droves of people got disabled as a result. We just ignored them and ignored their plight. ME/CFS happened, and we just ignored them and ignored their plight. And we are now caught unprepared for long COVID.

Faust: This is like three questions in one. I often think of COVID as kind of like we are present at a supernova, and then we're going to be living in the penumbra of that background radiation for the next billion years. It's never going to go away. And that every single coronavirus that we call a "seasonal coronavirus" now at one point in the past had that supernova, we just weren't present for it. Like you just described with influenza, 100 years ago humanity was present for that supernova.



Do you think that because of that, over time as the population gets more immunity and more exposures -- which is not good -- but over time, 50 years from now or even 10 years from now, that long COVID will become less likely as the population gains a sort of familiarity with it?

Al-Aly: It's possible. We don't know this for sure, obviously. I mean, we're trying to sort of forecast 10 years down the road. It's possible.

On one hand, it could be that the more immunity from repeated exposure could -- I mean that's a hypothesis, so it's very, very key to make sure that the audience knows this is a hypothesis, I don't have data for this -- will sort of make then coronavirus infection less intense, coronavirus infection inconsequential, clinically inconsequential.

But it is also possible that repeated exposure can, in some individuals, can also alter the immune system in some ways that make them actually more predisposed to a variety of adverse events down the road. It's really not clear, but I think this really deserves a lot more fleshing out and vetting over the next several years.



Remember we like sort of think about the pandemic -- this is only the fifth year. I mean, our understanding of all of this is still literally in its infancy.

Faust: And related to that, what is your current hypothesis on what the cause is?

I'll preface this by sharing a conversation I had with David Buller, who's one of the lead authors of the metformin trial that showed that if you take metformin during your acute illness, there was a big reduction in downstream long COVID. David was really convinced it's an antiviral property of metformin that is causing that.

And I said, "Well look, David, that may be true, but there also could be an anti-inflammatory component here -- that it's the body's immune reaction." And I was trying to convince him, I said, "I don't know the answer, but if it's an anti-inflammatory reaction, it's a bigger deal because that would actually suggest that metformin might help with other viruses that might cause longer-term syndromes."



Al-Aly: Yeah. So the David data is exciting, that finally something works. Metformin in the acute phase can actually reduce the risk of long COVID later on. We'd like to see that reproduced in other settings to elevate our confidence in that.

But going back to the mechanisms, at this point I sort of think that the viral persistence hypothesis is really compelling. There is clearly evidence, actually, in autopsy studies of people who have severe COVID-19 that there is viral persistence in extrapulmonary sites. Not only in the lung, but in the brain and in the coronary arteries, etc. So that sort of suggests that, at least in people who have severe disease -- that's not everyone -- the virus actually might persist for a long period of time in extrapulmonary sites.

There's also a lot of thinking and literature about that viral persistence potentially mediating some of the consequences that we see in long COVID.



The other hypothesis that I think is actually quite interesting is that of microbiome dysbiosis. So, viruses and bacteria actually interact. Viruses don't only attack human hosts or human or mammalian cells or human cells, viruses are indiscriminate. They go and wreak havoc in all our systems, and guess what, in our system there are actually more bacterial cells, more microbiome cells, than human cells. The idea is that those are in some way disturbed, that ecosystem is disturbed, and that subsequently might lead to disease.

The immune dysfunction hypothesis is actually very, very interesting. Recently work came out of [University of California, San Francisco]opens in a new tab or window, really a wonderful paper, describing discoordinated response between the T and B cells, and that discoordinated response is really what drives much of the manifestations that we see in long COVID.

I think the super clever finding in that interpretation -- beautiful, beautiful work -- is that this maybe explains why long COVID is a tissue-based disease.



So you think about why is long COVID not a heart disease only or a brain disease only, right? It's not organ specific; it's everywhere. There's no specificity. Actually, that's one of the things that really puzzled us at the beginning -- could this be true? Like, long COVID can do things in the heart and the brain and the GI [gastrointestinal] system and the kidneys -- that's not specific! But then they come up with a really clever explanation. If it's immune dysfunction, it can actually explain the tissue-based disease hypothesis. So that's also one other hypothesis that I think needs to also be fleshed out and evaluated further.

There is certainly inflammation during the acute phase -- things happen and subsequently an inflammatory cascade is then engaged and then that might result in post-acute sequela.

I have to say for the audience, these are hypotheses. We don't know that any of this really fully explains the human phenotype. A lot of these results are generated either in vitro, like totally cell-based data, or animal data. We don't really know if this really actually explains the human phenotype of long COVID.



But I'm really delighted to see this engagement by the research community, immunologists and virologists, to really decipher long COVID and try to help us understand what's happening here and how we can explain this very diverse phenotype. It's not only heart disease, not only brain disease, it's like all of the above. It's like, can this be true?

Because I'm pretty sure in training we also think of disease as an organ system-based disease. Even specialties are around cardiology, neurology, GI -- so even specialties are sort of based around organ systems, right? This is how our brain is trained. Even fellowships are organized around that concept. So this sort of challenges that a little bit because it's literally a multi-system disorder.

Faust: Yeah. I mean, it reminds me as an emergency physician of sepsis in a way. In terms of that it's not necessarily just the virus or just the pathogen. It's the host response to that, and that can be anywhere, anywhere you have an immune tissue in your body -- which is everywhere, head to toe.

"

 

[missy]

"

Newborns Better Protected With 3 Doses of Maternal COVID Vaccine​

— And cord anti-S antibody levels were the same for preterm and full-term pregnancies, study shows​

by Katherine Kahn, Staff Writer, MedPage Today January 19, 2024

For pregnant people, three doses of an mRNA COVID-19 vaccine resulted in 10-fold higher antibody levels in umbilical cord samples of preterm and full-term deliveries compared with only two doses, a prospective cohort study showed.
Geometric mean concentration of cord SARS-CoV-2 anti-Spike (anti-S) antibodies increased from 1,000 after two doses of vaccine to 9,992 for those who received three or more doses (P<0.001), reported Alisa Kachikis, MD, of the University of Washington in Seattle, and colleagues in JAMA Network Openopens in a new tab or window.

In addition, concentrations of SARS-CoV-2 anti-S antibodies in paired maternal blood samples significantly increased, from 674 in those who received two vaccine doses to 8,159 in those who received 3 or more doses (P<0.001).
Notably, cord anti-S antibody levels were similar in preterm and full-term pregnancies, with geometric mean concentrations of 8,818 and 10,423, respectively (P=0.34). After adjusting for vaccine timing and dose number before delivery, there was no association between preterm delivery and cord anti-S antibody levels (β=0.44, 95% CI -0.06 to 0.94).
"We were surprised that, when adjusted for vaccine dose number and time from last vaccine dose, preterm babies received similar benefit from COVID-19 vaccines given to their mothers compared to term babies," Kachikis told MedPage Today. "It shows that maternal antibody concentrations matter and we should consider high-risk pregnancies when thinking about timing of vaccines during pregnancy."
For both preterm and full-term pregnancies, the median time between last vaccine dose and delivery was 16 weeks, and the median gestational age at last vaccine dose was 25 weeks.

"Changes in antibody levels didn't really seem to correlate much with gestational age at the time of birth, so we shouldn't necessarily time a booster injection to the last few weeks of pregnancy thinking that's going to be most protective for the newborn," Angela Bianco, MD, director of maternal-fetal medicine at the Icahn School of Medicine at Mount Sinai in New York City, told MedPage Today. "We probably should encourage women even earlier in pregnancy or at the outset of pregnancy to get boosted if they haven't already."
A study from October showed that maternal mRNA COVID-19 vaccination during pregnancy protected young infants opens in a new tab or windowfrom COVID-related hospitalization, and another study found that maternal vaccination lowered risks of poor neonatal outcomesopens in a new tab or window. However, a recent CDC surveyopens in a new tab or window showed that although 58.7% of pregnant women had completed the primary COVID vaccination series, only 27.3% reported receiving an updated booster dose before or during their current pregnancy.

The current study enrolled 220 pregnant individuals at the University of Washington from February 2021 through January 2023. All had received at least two doses of mRNA COVID vaccine before giving birth and had no history of prior COVID infection (confirmed by the absence of anti-SARS-CoV-2 nucleocapsid antibodies at delivery). The median age of participants was 34 years, and approximately 82% were white.
Among participants, 121 received two doses of an mRNA vaccine and 99 received three or more vaccine doses, before or during pregnancy. Of the 36 preterm deliveries, the median gestational age was 35.1 weeks, but ranged from approximately 28 to 37 weeks, including 19.4% delivered at less than 34 weeks. The 184 full-term infants were delivered at a median 39.5 weeks. Cesarean section delivery was more common among preterm infants than those carried to full term (66.7% vs 35%, respectively).
Kachikis and colleagues noted that the study was limited by its small sample size. Because selection criteria required participants to have received at least two doses of an mRNA vaccine, the study population was limited to those with high vaccine acceptance rates.

Bianco also noted that the study population was mostly white individuals with private health insurance who had never had COVID. Additionally, very few early preterm deliveries were included and the researchers did not specify the causes of preterm deliveries. These factors mean the findings of the study might not apply to other populations, she explained.

• 
  
  Katherine Kahn is a staff writer at MedPage Today, covering the infectious diseases beat. She has been a medical writer for over 15 years.
• 
  
• "

 

[missy]

"
Medscape Medical News

Ophthalmology

​

Why Are Women More Likely to Get Long COVID?​

January 19, 2024


Annette Gillaspie, a nurse in a small Oregon hospital, hoped she would be back working with patients by now. She contracted COVID-19 on the job early in the pandemic and ended up with long COVID.
After recovering a bit, her fatigue and dizziness returned, and today she is still working a desk job. She has also experienced more severe menstrual periods than before she had COVID.
"Being a female with long COVID definitely does add to the roller-coaster effect of symptoms," Gillaspie said.

Long COVID affects nearly twice as many women as men, with 6.6% of women reporting long COVID compared with 4% of men, according to a recent Census Bureau survey reported by the Centers for Disease Control and Prevention (CDC). Researchers are trying to determine why, what causes the gender disparity, and how best to treat it.
Scientists are also starting to look at the impact of long COVID on female reproductive health, including menstruation, pregnancy, and menopause.


Sex differences are common in infection-associated illnesses, said Beth Pollack, a research scientist specializing in long COVID in the Massachusetts Institute of Technology's Department of Biological Engineering, Cambridge, Massachusetts. "It informs research priorities and the lens with which we understand long COVID."

For example, reproductive health issues for women, such as puberty, pregnancy, and menopause, can alter the course of illness in a subset of women in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and postural orthostatic tachycardia syndrome (POTS), a condition that can cause dizziness and worse.
"This suggests that sex hormones may play key roles in immune responses to infections," Pollack said.
ME/CFS and a Possible Link to Long COVID in Women

Some of the research into long COVID is being led by teams studying infection-associated chronic illnesses like ME/CFS.
The problem: Advocates say ME/CFS has been under-researched. Poorly understood for years, the condition is one of a handful of chronic illnesses linked to infections, including Lyme disease and now long COVID. Perhaps not coincidently, they are more likely to affect women.
Many of the research findings about long COVID mirror data that emerged in past ME/CFS research, said Jaime Seltzer, the scientific director at #MEAction, Santa Monica, California, an advocacy group. One point in particular: ME/CFS strikes women about twice as much as men, according to the CDC.
Seltzer said the response to long COVID could be much further ahead if the research community acknowledged the work done over the years on ME/CFS. Many of the potential biomarkers and risk factors emerging for long COVID were also suspected in ME/CFS, but not thoroughly studied, she said.
She also said not enough work has been done to unravel the links between gender and these chronic conditions.
"We're stuck in this Groundhog Day situation," she said. "There isn't any research, so we can't say anything definitively."
Some New Research, Some New Clues
Scientists like Pollack are slowly making inroads. She was lead author on a 2023 review investigating the impact of long COVID on female reproductive health. The paper highlights long COVID links to ME/CFS, POTS, and Ehlers-Danlos syndrome (EDS), as well as a resulting laundry list of female reproductive health issues. The hope is physicians will examine how the menstrual cycle, pregnancy, and menopause affect symptoms and illness progression of long COVID.
The Tal Research group at MIT (where Pollack works) has also added long COVID to the list of infection-associated illnesses it studies. The lab is conducting a large study looking into both Lyme disease and long COVID. The goals are to identify biomarkers that can predict who will not recover and to advance available treatments.
Another MIT program, "SEXX + Immunity" holds seminars and networking sessions for scientists looking into the role of female and male biology in immune responses to infection.
Barriers to Progress Remain
On the clinical side, female patients with long COVID also have to deal with a historical bias that still lurks in medicine when it comes to women's health, said Alba Azola, MD, an assistant professor of physical medicine at Johns Hopkins Medicine, Baltimore, Maryland.

Azola said she has discovered clinical descriptions of ME/CFE in the literature archives that describe it as "neurasthenia" and dismiss it as psychological.
Patients say that it is still happening, and while it may not be so blunt, "you can read between the lines," Azola said.
Azola, who has worked with long-COVID patients and is now seeing people with ME/CFS, said the symptoms of infection-associated chronic illness can mimic menopause, and many of her patients received that misdiagnosis. She recommends that doctors rule out long COVID for women with multiple symptoms before attributing symptoms to menopause.
Seeing that some long-COVID patients were developing ME/CFS, staff at the Bateman Horne Center in Salt Lake City, Utah, set up a program for the condition in 2021. They were already treating patients with ME/CFS and what they call "multi-symptom chronic complex diseases."
Jennifer Bell, a certified nurse practitioner at the center, said she has not seen any patients with ovarian failure but plenty with reproductive health issues.
"There definitely is a hormonal connection, but I don't think there's a good understanding about what is happening," she said.

Most of her patients are female, and the more serious patients tend to go through a worsening of their symptoms in the week prior to getting a period, she said.
One thing Bell said she's noticed in the past year is an increase in patients with EDS, which is also more common in women.
Like long COVID, many of the conditions traditionally treated at the center have no cure. But Bell said the center has developed an expertise in treating post-exertional malaise, a common symptom of long COVID, and keeps up with the literature for treatments to try, like the combination of guanfacine and the antioxidant N-acetyl cysteine to treat brain fog, an approach developed at Yale.
"It's a very challenging illness to treat," Bell said.
Since the emergence of long COVID, researchers have warned that symptoms vary so much from person to person that treatment will need to be targeted.
Pollack of MIT agrees and sees a big role for personalized medicine.
We need to "identify phenotypes within and across these overlapping and co-occurring illnesses so that we can identify the right therapeutics for each person," she said.
As for Annette Gillaspie, she still hopes her long COVID will subside so she can get out from behind the desk and return to her normal nursing duties.
"I just got to a point where I realized I'm likely never going to be able to do my job," she said. "It was incredibly heart breaking, but it's the reality of long COVID, and I know I'm not the only one to have to step away from a job I loved."



"

 

[Daisys and Diamonds]

Breaking Down the Latest on Long COVID Research​

— Ziyad Al-Aly, MD, explains long COVID symptoms, potential causes, and why it's so hard to study​

by Jeremy Faust, MD, MS, MA, Editor-in-Chief, MedPage Today ; Emily Hutto, Associate Video Producer January 19, 2024
Jeremy Faust, MD, editor-in-chief of MedPage Today, and Ziyad Al-Aly, MD, chief of the Research and Education Service at the VA St. Louis Health Care System in Missouri, discuss the latest long COVID research and what it could mean for potential future treatments.

The following is a transcript of their remarks:

"

Faust: My first question is how many different diseases do you think long COVID is? Is it one, is it two, is it five? What do you think?



Al-Aly: Well, long COVID is really a multi-systemic disease. There's no one long COVID; there are likely to be many subtypes.

Our understanding of long COVID now is actually literally embryonic. It's in its infancy. We've made a lot of progress over the past several years, but we need to also recognize that we've only been researching this and understanding long COVID for literally only 4 years.

I tell people when we first started thinking and discovering neoplasm or tumor growth or cancer, we sort of defined, "Oh, this is a lump," or, "This is a cancer" -- and now we have 800 different types of cancer because we understand the biology more. We understand the molecular and genetic fingerprints of cancer much more deeply. We understand tissue-based biology of cancer much more deeply than we did, let's say, 50 years ago. And long COVID is the same thing.



Long COVID is really this post-viral illness or the lingering or enduring problems that happen after SARS CoV-2 infection. We know so far it can affect nearly every organ system. It can affect the heart, the brain, can have metabolic sequela and we're starting to see studies subtyping long COVID into different types.

There are cardinal manifestations that a lot of the audience might have heard of: brain fog, fatigue, post-exertional malaise, or some form of dysautonomia, or postural orthostatic tachycardia syndrome [POTS], or more broadly dystonia or a dysfunction in the autonomic nervous system that would lead to subsequent manifestation. Those are the cardinal manifestations. But really, there is no organ in the body now, 4 years into it, that long COVID does not touch.

Faust: One of the audience questions was whether you see a similarity between long COVID and ME/CFS, myalgic encephalomyelitis/chronic fatigue syndrome. And I'm really interested in this because on one hand I could see it being a good framework to understand these conditions as similar, but also could be a disservice if they're different. What do you think?



Al-Aly: I think there's a lot of overlap.

I mean, ME/CFS itself -- to start with the origin of ME/CFS -- is also thought to be triggered by a viral illness, by a flu-like illness. The onset of ME/CFS doesn't happen in a vacuum. It actually is triggered initially by a viral illness. So, there are likely common etiologic drivers. It may not be the same virus, but it is triggered by a viral illness.

There's a lot of overlap in the symptomatology -- fatigue, brain fog, post-exertional malaise, POTS -- there's quite a bit of overlap in the symptomatology between ME/CFS and long COVID.

It doesn't mean that all the facets are identical. It just means that it sort of gives us hints. The viruses are giving us hints that the viruses we thought initially only caused acute problems or acute disease can in some instances lead to chronic illness or chronic disease. ME/CFS is one example, COVID is another example.



And one of the arguments that I actually find really interesting is that had we as a community of scientists listened to ME/CFS patients a long time ago and really understood it better and [did] more research on it, we'd actually be better and more equipped and more able to address the challenges of long COVID more. We just ignored it. We literally had the Spanish flu pandemic, droves of people got disabled as a result. We just ignored them and ignored their plight. ME/CFS happened, and we just ignored them and ignored their plight. And we are now caught unprepared for long COVID.

Faust: This is like three questions in one. I often think of COVID as kind of like we are present at a supernova, and then we're going to be living in the penumbra of that background radiation for the next billion years. It's never going to go away. And that every single coronavirus that we call a "seasonal coronavirus" now at one point in the past had that supernova, we just weren't present for it. Like you just described with influenza, 100 years ago humanity was present for that supernova.



Do you think that because of that, over time as the population gets more immunity and more exposures -- which is not good -- but over time, 50 years from now or even 10 years from now, that long COVID will become less likely as the population gains a sort of familiarity with it?

Al-Aly: It's possible. We don't know this for sure, obviously. I mean, we're trying to sort of forecast 10 years down the road. It's possible.

On one hand, it could be that the more immunity from repeated exposure could -- I mean that's a hypothesis, so it's very, very key to make sure that the audience knows this is a hypothesis, I don't have data for this -- will sort of make then coronavirus infection less intense, coronavirus infection inconsequential, clinically inconsequential.

But it is also possible that repeated exposure can, in some individuals, can also alter the immune system in some ways that make them actually more predisposed to a variety of adverse events down the road. It's really not clear, but I think this really deserves a lot more fleshing out and vetting over the next several years.



Remember we like sort of think about the pandemic -- this is only the fifth year. I mean, our understanding of all of this is still literally in its infancy.

Faust: And related to that, what is your current hypothesis on what the cause is?

I'll preface this by sharing a conversation I had with David Buller, who's one of the lead authors of the metformin trial that showed that if you take metformin during your acute illness, there was a big reduction in downstream long COVID. David was really convinced it's an antiviral property of metformin that is causing that.

And I said, "Well look, David, that may be true, but there also could be an anti-inflammatory component here -- that it's the body's immune reaction." And I was trying to convince him, I said, "I don't know the answer, but if it's an anti-inflammatory reaction, it's a bigger deal because that would actually suggest that metformin might help with other viruses that might cause longer-term syndromes."



Al-Aly: Yeah. So the David data is exciting, that finally something works. Metformin in the acute phase can actually reduce the risk of long COVID later on. We'd like to see that reproduced in other settings to elevate our confidence in that.

But going back to the mechanisms, at this point I sort of think that the viral persistence hypothesis is really compelling. There is clearly evidence, actually, in autopsy studies of people who have severe COVID-19 that there is viral persistence in extrapulmonary sites. Not only in the lung, but in the brain and in the coronary arteries, etc. So that sort of suggests that, at least in people who have severe disease -- that's not everyone -- the virus actually might persist for a long period of time in extrapulmonary sites.

There's also a lot of thinking and literature about that viral persistence potentially mediating some of the consequences that we see in long COVID.



The other hypothesis that I think is actually quite interesting is that of microbiome dysbiosis. So, viruses and bacteria actually interact. Viruses don't only attack human hosts or human or mammalian cells or human cells, viruses are indiscriminate. They go and wreak havoc in all our systems, and guess what, in our system there are actually more bacterial cells, more microbiome cells, than human cells. The idea is that those are in some way disturbed, that ecosystem is disturbed, and that subsequently might lead to disease.

The immune dysfunction hypothesis is actually very, very interesting. Recently work came out of [University of California, San Francisco]opens in a new tab or window, really a wonderful paper, describing discoordinated response between the T and B cells, and that discoordinated response is really what drives much of the manifestations that we see in long COVID.

I think the super clever finding in that interpretation -- beautiful, beautiful work -- is that this maybe explains why long COVID is a tissue-based disease.



So you think about why is long COVID not a heart disease only or a brain disease only, right? It's not organ specific; it's everywhere. There's no specificity. Actually, that's one of the things that really puzzled us at the beginning -- could this be true? Like, long COVID can do things in the heart and the brain and the GI [gastrointestinal] system and the kidneys -- that's not specific! But then they come up with a really clever explanation. If it's immune dysfunction, it can actually explain the tissue-based disease hypothesis. So that's also one other hypothesis that I think needs to also be fleshed out and evaluated further.

There is certainly inflammation during the acute phase -- things happen and subsequently an inflammatory cascade is then engaged and then that might result in post-acute sequela.

I have to say for the audience, these are hypotheses. We don't know that any of this really fully explains the human phenotype. A lot of these results are generated either in vitro, like totally cell-based data, or animal data. We don't really know if this really actually explains the human phenotype of long COVID.



But I'm really delighted to see this engagement by the research community, immunologists and virologists, to really decipher long COVID and try to help us understand what's happening here and how we can explain this very diverse phenotype. It's not only heart disease, not only brain disease, it's like all of the above. It's like, can this be true?

Because I'm pretty sure in training we also think of disease as an organ system-based disease. Even specialties are around cardiology, neurology, GI -- so even specialties are sort of based around organ systems, right? This is how our brain is trained. Even fellowships are organized around that concept. So this sort of challenges that a little bit because it's literally a multi-system disorder.

Faust: Yeah. I mean, it reminds me as an emergency physician of sepsis in a way. In terms of that it's not necessarily just the virus or just the pathogen. It's the host response to that, and that can be anywhere, anywhere you have an immune tissue in your body -- which is everywhere, head to toe.

"

i just heard this on the news yesterday afternoon

Long Covid care gains seen from data

A pilot study of long Covid and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has confirmed the two conditions are closely related....

www.odt.co.nz

 

[Daisys and Diamonds]

my boss had to take her hubbie to hospital last week (blood clot in lung after surgery for a hernia before xmas) and she picked up some free tests for me

Covid cases rising as Govt looks to end free rapid antigen tests

The imminent end to funding comes as 8000 new Covid cases were reported last week and daily infections are the highest in six months.

www.1news.co.nz

her hubbie is ok now after 5 days in hospital

 

[missy]

"

How to (and not to) boost your immune system​

KATELYN JETELINA AND DR. ANDREA LOVE JAN 25 ∙

​

The rumor mill is hot with ways to “boost your immune system” this viral season. Legitimate and illegitimate claims on prevention and treatment are entangled on social media and massive podcasts (cough, cough Huberman), making it almost impossible to navigate.
So we pulled together this list for you: What works? What doesn’t work? And why?

Note: The following is just a snippet of a larger document, which can be downloaded at the end of this post.

What works?​

If you get symptoms, the best thing you can do is give your immune system time to do its job.
Vaccines can help by reducing viral load, and antivirals can also help stop the virus from replicating. But of the 200+ viruses circulating right now, not all have vaccines or antivirals.
What else can help?

• A balanced, nutrient-dense diet. We are not at the point where a diet or specific foods can be recommended to ensure an optimally functioning immune system. This is because our immune system is complex and relies on a balance of many factors. In general, focus on diets rich in produce, fiber, whole grains, lean proteins, and vegetable oils. The most robust evidence of a nutrient-based diet is on specific health outcomes (like stroke, hypertension, or heart disease). However, there are meta-analyses showing a positive, direct impact on the immune system, too.
• Sleep is critical, as this is when the immune system executes most of its repair processes. This includes the production and regulation of important chemicals required for immune cell function, communication, and tissue regeneration. Those who are chronically sleep-deprived are shown to get colds more often than those who aren’t.
  

  ​

  (Source: CDC)
• Hydration. Proper fluid balance ensures your body can transport nutrients and immune cells and remove pathogens and waste products (via draining lymph nodes). In addition, proper hydration allows your mucous membranes to maintain their protective barriers.

What does not work?​

Many other immune health remedies land in one of three categories:

1. No evidence of working despite being tested repeatedly
2. Little evidence either way
3. Weak evidence for one thing, but claims are exaggerated

Here are the most popular misconceptions:

1. You do not need to get re-infected to keep your immune system active. Contrary to rumors, we don’t need to get re-infected over and over for our immune systems to be ready to respond. Everything in our life—our house, pets, our own body—is filled with microbes. Although these microbes aren’t harmful, they share enough structural similarities with dangerous microbes to keep our immune systems active and ready to defend against dangerous foreign invaders. Infection doesn’t aid in that.
2. For the general population, dietary supplements do not work in preventing or reducing the severity of illness. Ingesting one nutrient only benefits those with a substantial deficiency or in a specific subpopulation (e.g., pregnant, lactating). What about…
   • Vitamin C? A balanced diet can readily obtain the necessary levels to support immune function. There are a lot of misconceptions about megadosing vitamin C for sickness, which stemmed from three things: 1. Vitamin C prevented scurvy in sailors a long time ago, which suggested some role. 2. A book in the 1970s supercharged this misconception with common colds. 3. Some animal studies and small but poorly conducted human studies are often cited as proof.
   • Vitamin D? Very low vitamin D levels can reduce your ability to deal with respiratory infections, but this level of deficiency is very uncommon in high-income nations like the United States. A recent meta-analysis of randomized controlled trials found that vitamin D supplementation did not impact respiratory illness among subgroups. Only when data were pooled was a small effect (1%) noted, which is unlikely to have clinical relevance.

   • ​

   • Iron? This is critical for immune system function, but paradoxically, it is also critical for many pathogens to do their job. Iron deficiency is most common among women and children, particularly in low-income countries. A medical provider should manage legitimate deficiencies, as iron supplement compositions are not regulated and vary widely.
   • Probiotics? These are dietary supplements that contain live microorganisms, such as bacteria. No evidence suggests that people with normal gastrointestinal tracts can benefit from probiotics for respiratory health. There may also be risks for with individuals with compromised defenses, like children. (There was a recent warning from the FDA to probiotic company after the death of a child.)

There are two problems with supplements:

1. They aren’t regulated for safety or efficacy. This means that even if you’re buying the same exact supplement from the same exact company, there is variability in the quality, formulation, and bioavailability (i.e., how much is available for your body to use). There can be too much of a good thing, and supplements are a great example.
2. The placebo effect is real. For example, in a randomized control study of multivitamins, the intervention group reported better health despite no apparent differences in health outcomes. Another studyon sham diet supplements found the same and concluded the placebo effect is even more disadvantageous when the first line of treatment is behavioral.

What else doesn’t work?​

• Cold plunges or ice baths are increasingly popular for “boosting” immunity, but there is inconclusive evidence based on small and conflicting studies. For example, one study of 10 athletes observed a small increase in white blood cell concentrations in blood after many cold plunges in a row (which one could argue may aid immune function), but another study found it didn’t. One randomized control trial in the Netherlands found cold plunges reduced sickness absences from work by 30%, but not the number of days of feeling crummy. The benefits have to outweigh the risks, too. Sudden immersion in water under 60°F can kill a person in <1 minute and cause cardiovascular stress, especially for those with underlying health issues.

​

• Nasal breathing is a recently popularized phenomenon built off the idea that breathing through your nose is better for your immune system than breathing through the mouth. While it is true that nasal breathing can increase nitric oxide levels (an important molecule for the immune system to function), there is limited evidence of the real-world impact. Nasal breathing is not the primary route of nitric oxide: it’s generated via countless other processes and through the consumption of foods, particularly leafy greens. Nasal breathing has been noted to have some benefits for specific populations like patients recently intubated.
• Saunas are often purported to sweat out toxins, boost immunity, and more. However, the evidence is limited. The commonly cited study used to justify saunas has serious limitations. For example, the study population was small (20 people), all men, and young (20-25). People with the money to afford a sauna or a gym with a sauna are often higher income, likely to exercise and have access to high-quality foods. Also, while they report statistically significant differences after the sauna, the data overlap.

In summary ​

We have a few tools to help prevent and treat viral illnesses. However, the best tool we have is our immune systems. Our body does a great job of keeping that tip-top shape without fads. Stay healthy out there!


"

 

[missy]

"

State of Affairs: Jan 23​

KATELYN JETELINA JAN 23

Anddddd respiratory illnesses have peaked. This means we are in the smack middle of the season, as we still need to go down the wave.

Here is your state of affairs.

Influenza-like illnesses: High but declining​

The number of people seeking healthcare for respiratory illnesses—fever, cough, or sore throat symptoms—is still high but declining rapidly. In previous years, we’ve seen multiple humps, so don’t be surprised if this starts increasing again.

​

Outpatient Respiratory Illness Visits (Source: CDC; Annotated by YLE)
If we look at the “big three,” flu, RSV, and Covid-19 have seen improvement. Flu is causing the most symptom burden, while Covid-19 continues to lead to severe disease.

Given that we are at the peak of the season, how is healthcare capacity? It is incredibly difficult (if not impossible) to gauge through data. This is because what happens internally (diverting care, delayed election surgeries, increased staffing for more beds, expedited discharge planning) isn’t reflected by numbers reported by hospitals. So we rely on anecdotes on the ground, like this one from Boston-based Massachusetts General Hospital a few days ago:

Almost four years after the start of the COVID-19 pandemic, Massachusetts General Hospital … continues to struggle daily with unprecedented overcrowding – particularly in its Emergency Department (ED). For the past 16 months, the MGH ED has operated nearly every day in “Code Help” or “Capacity Disaster” status.

This is concerning because it’s poorly timed with burnout and staff shortages. This will impact everyone’s care. We must figure this out if this is the “new normal.”

Now, a deeper dive into the “big three.”

Covid-19: Very high but declining​

Covid-19 wastewater activity is still “very high.” In fact, it’s higher than it was last year. However, on a national level, activity is declining quickly. This basically means the newest subvariant (JN.1) is running out of new infection pathways.

There is still a lot of variability on the local level. For example, many cities—like San Jose, Chicago, and Miami—have yet to peak.

​

Wastewater SARS-CoV-2 viral activity level on a national level (Source: CDC; Annotations by YLE)
Covid-19 continues to be the leader in severe disease, like hospitalizations. Covid-19 is currently causing about 3 times more deaths than the flu.

​

It doesn’t have to be like this. Covid-19 vaccination rates remain abysmal (41% among those over 65 compared to 75% flu vaccine coverage). If we look at the UK, where more than 70% of the eligible population is vaccinated for Covid-19, flu hospitalizations passed those for Covid-19 this season.

​

Figure Source: Prof Christina Pagel; Annotated by YLE

Flu: High and stabilizing​

Flu peaked around New Year’s and started to decline quickly. However, we typically see patterns disrupted once school starts again, which happened this year. Flu rates stabilized among kids 5-17 years old, while the other age groups continued to decline.

​

Percent of Emergency Department Visits for Flu, by age. (Source CDC; Annotated by YLE)
There have been 47 pediatric deaths due to flu so far this season.

RSV: Moderate and declining​

RSV numbers remain higher than this time last year but continue to decline.

​

National percent positivity rate of RSV tests (Source: CDC)
Hospitalizations among young children are nosediving. Adult RSV patterns are following pediatrics (as usual).

​

RSV hospitalization rates by age (Source: CDC; Annotations by YLE)

Other things I’m paying attention to​

• Spring vaccines? Many people are asking whether we will have spring Covid-19 vaccines for those over 65 again. I don’t know. But I do know that CDC’s advisory board—ACIP—has their regularly scheduled meeting at the end of February. I will keep you updated.
• Measles. Beyond those discussed in the previous YLE post, another outbreak was reported in Washington state (6 measles cases linked to a family gathering). In addition, the U.K. Health Security Agency (UKHSA) declared a national incident for measles, which is a strong signal showing increased concern. Currently, 319 measles cases are linked to an outbreak in the West Midlands.
• Charcuterie meats. The CDC warned of a Salmonella outbreak linked to charcuterie meats. They’re advising the public not to eat the Busseto Charcuterie Sampler from Sam’s Club or the Fratelli Beretta brand Antipasto Gran Beretta from Costco.

Bottom line​

There is still a lot of sickness out there, but we are finally headed towards relief. One can’t help but wonder how this season, particularly the strain on hospitals today, would be different if more people got vaccinated.

Stay healthy out there!




"

 

[missy]

Evolution of the human immune system in the post-Omicron era | MDLinx

www.mdlinx.com

“

Evolution of the human immune system in the post-Omicron era​

Published January 22, 2024 | Originally published on MedicalXpress Breaking News-and-Events
It has been four years since the start of the COVID-19 pandemic. SARS-CoV-2 has yet to be eradicated and new variants are continuously emerging. Despite the extensive immunization programs, breakthrough infections (infection after vaccination) by new variants are common.
New research suggests that human immune responses are also changing in order to combat the never-ending emergence of new SARS-CoV-2 variants. Specifically, it has been discovered the immune system that encountered breakthrough infection by the omicron variant acquires enhanced immunity against future versions of the omicron. The study is published in Science Immunology.
CME Activity: Oncology Innovations: Liquid Biopsy in Lung Cancer Management RealCME
A team of South Korean scientists led by Professor Shin Eui-Cheol of the Korea Virus Research Institute Center for Viral Immunology within the Institute for Basic Science (IBS) announced that the memory T cells that form during the omicron breakthrough infection respond to subsequent strains of the virus.
Emerging in late 2021, the SARS-CoV-2 omicron variant had drastically increased transmissibility in comparison to its predecessors, which quickly allowed it to become the dominant strain in 2022. New strains of omicron have kept emerging ever since then. Starting with BA.1 and BA2, BA.4/BA.5, BQ.1, XBB strains, and more recently JN.1 strains were among the new strains of the omicron variant. This has led to widespread breakthrough infection despite vaccination.
After becoming infected or vaccinated, the body creates neutralizing antibodies and memory T cells against the virus. The neutralizing antibody serves to prevent host cells from being infected by the virus. While memory T cells cannot prevent the infection, they can quickly search and destroy infected cells, preventing the viral infection from progressing into a severe disease.
The research team's goal was to find out the changes that occur in our body's immune system after suffering from post-vaccination breakthrough infection. In order to answer that question, they focused on the memory T cells that formed after the omicron infection.
The previous studies on the omicron variant have mostly focused on vaccine efficacy or neutralizing antibodies, and the research related to memory T cells has been comparatively lacking.
The research team selected patients who suffered then recovered from BA.2 omicron breakthrough infection in early 2022 as subjects and conducted studies on their memory T cells, specifically in their ability to respond to various omicron variants such as BA.2, BA.4/BA/5, and others.
In order to do so, immune cells were separated from the peripheral blood of the subjects, and the memory T cells' cytokine production and anti-viral activities in response to various spike proteins from different variants were measured.
The results showed that the memory T cells from these patients showed heightened response against not only the BA.2 strain but the later BA.4 and BA.5 strains of omicron as well. By suffering from breakthrough infection, these patients' immune system was strengthened to combat future strains of the same virus.
The research team also discovered the specific part of the spike protein which is the primary cause of the observed enhancement in the memory T cells. These results show that once a person undergoes breakthrough infection by the omicron infection, it is unlikely for them to ever suffer severe COVID-19 symptoms from the future emerging variants.
Research Fellow Jung Min Kyung who led this research stated, "This finding gives us new perspectives in the new era of COVID endemic," adding, "It can be understood that in response to constant emergence of new virus variants, our bodies have also adapted to combat the future strains of the virus."
Director Shin Eui-Cheol of the Center for Viral Immunology commented, "This new finding can also be applied to vaccine development. By searching for common features among the current dominant strain and emerging new strains of viruses, there may be higher chances to induce memory T cell defenses against the subsequent variants."
This research has been conducted in collaboration with colleagues from Yonsei University Severance Hospital, Korea University Hospital, Sungkyunkwan University, and Samsung Medical Center”

 

[missy]

"

The Real COVID Isolation Headline That Nobody Is Picking Up On​

— Hint: It relates to you, California healthcare worker​

by Jeremy Faust, MD, MS, MA, Editor-in-Chief, MedPage Today January 25, 2024

• 
  
  Jeremy Faust is editor-in-chief of , an emergency medicine physician at Brigham and Women's Hospital in Boston, and a public health researcher. He is author of the Substack column Inside Medicine. Follow

California has a new COVID-19 isolation guideline that differs from the CDC's. Under its new policyopens in a new tab or window, California residents with confirmed COVID-19 can end their isolation once they have not had a fever (without fever-reducing medication) for 24 hours and other symptoms are improving. In addition, asymptomatic patients do not need to isolate at all. Masking for 10 days is deemed sufficient.
Many of you have been asking me about this. Including The Boston Globe. First, I'll share my quotes from an articleopens in a new tab or window on this in the Globe earlier this week. Then we'll go deeper.

• California's new policy is an example of harm reduction, which is an important concept. "When people are going to do something or nothing, you offer something they are more likely to do." The idea here is that given pandemic fatigue (this is year five), it's better to ask people something they'll do, rather than ignore a larger ask...but...
• That said, "I don't know how they came up with this. I suspect that they just chose something that people could remember." That's trouble, potentially. On one hand, the science isn't ironclad here. People without a fever have lower viral loads, but that's not airtight. So, I tend to think that the scientists behind this policy took some things that are true, and applied them broadly. Look, asymptomatic cases are probably less contagious. There's decent data for that. But asymptomatic is not the same thing as presymptomatic. When my colleague Michael Mina, MD, PhD, says, "symptoms do not reflect infectivity, and they never have," I mostly agree. You can have tons of symptoms and not be contagious. But it is also true that completely asymptomatic cases tended to have lower viral loads.
• Presymptomatic COVID-19, however, poses a real problem. This is my biggest issue with California's guidance. "You may have no symptoms until day three or four, and by that time your viral loads are off the charts, and you're a super spreader," I told the Globe. The problem is that California lets people who tested positive for COVID-19 but are not yet symptomatic roam free, albeit in a mask. That may be fine at first. But some will have their viral loads enter an exponential growth phase (i.e., go from not contagious to extremely contagious in a short period) just as symptoms may be starting to appear. These are preventable super spreaders that the new guidance does nothing about, and could make worse.
• If your rapid COVID-19 test line is bright (brighter than the control line), and the test turns positive quickly, "I don't care what symptoms you have, you need to isolate." As I've written here before, the brightness of your test line has meaning. A bright and fast result means you are likely extremely contagious. (The meaning when the results are positive but less dramatic are a little more complicated; you're likely still contagious to some degree, but the magnitude is harder to know.)

What Didn't Make It Into the Globe (and the Headline Nobody Is Picking Up On...)
I had more to say to the Globe's health journalist Adam Piore, but not everything can fit into the paper. So, here are some further thoughts I have that we touched on during our conversation earlier this week:
More on harm reduction. People who are truly asymptomatic are probably less contagious, but they still may be contagious at times. People who no longer have a fever are less contagious than those with fever; but they still may be contagious. Yes, something is better than nothing; I am just not sure where they got this particular "something."
To be fair, the California guidance is all based on true things. The question is whether this policy effectively decreases spread or not. It might -- and if the scientists have modeling for this, I'd love to see the results. But I'm worried that any modeling they performed may have badly misunderstood the distinction between asymptomatic and pre-symptomatic cases, and the unique implications that these situations carry.

Why you tested matters. It's one thing if you get a positive test after a couple days of symptoms. In that context, California's guidance is based on data that show that decreasing viral loads often (but not always) correlate to reductions in symptoms. But if you tested positive because your roommate has COVID-19 and you're worried you might have caught it from them, this guidance misses the mark and potentially lets you become a superspreader. For example, if you test positive a couple days after an exposure but do not have symptoms, you don't know when your viral load will start going exponential (the time when you're at highest risk of spreading the virus) and whether symptoms will appear just before, during, after that phase, or never.
Context matters. Some degree of spread of COVID-19 on a college campus is a lot more tolerable than some degree of spread in healthcare facilities like nursing homes or acute rehab facilities where your dad goes after that hip replacement. Which leads to...

This next one should have been a headline. (In fairness, I hadn't fully noticed this myself when I spoke to the Globe.) The California guidance actually implies, but does not explicitly state, that many or most healthcare workers should not go to work for 10 days after a positive COVID-19 test. It says, "Avoid contact with those who are at higher risk for severe COVID-19 for 10 days." To me, that says that healthcare workersshould not see many of their patients during that time. I wholeheartedly agree.
If there is any thing we 100% must be doing, it is preventing the spread of this virus to the highest-risk individuals. Healthcare workers and others who work closely with high-risk populations need to get paid sick leave to cover their contagious windows (ideally, as determined by two negative rapid antigen tests, taken a day apart). If California were to enforce this part of its guidance (will they?) I would actually be far more willing to accept the rest of the guidance's gambles. But I doubt they will, nor is it feasible given the lack of financial support to (and therefore by) healthcare institutions at this point in the pandemic.

Concluding Thoughts
Look around. Everywhere you go, people are not doing much to prevent the spread of COVID-19. It's year five of the pandemic and deaths and hospitalizations are a lot lower. I get it. Still, I wish people would mask in some situations. (Like, why not mask in super crowded spaces where nobody is talking anyway?) But it is not happening on a large scale. Nor are most people abiding by the CDC's isolation guidelinesopens in a new tab or window at this point.
So, we want to find a way to maximally reduce spread -- especially to key populations -- with minimal disruption. The fever rule may help; but it could backfire if too many afebrile people now go out and spread this thing. The asymptomatic rule may turn out to be not too hazardous (though, again, I worry about the pre-symptomatics); but really, I hope infected asymptomatic people who choose not to isolate will wear N95 masks when they go out. (And for concerned readers: one-way N95 masking drastically reduces your chances of getting COVID-19.)

More than that, though, that California (and Oregon) are going rogue from the CDC's guidelines reflects something larger: Times have changed, and so should the guidelines. Yes, harm reduction is indeed a better strategy than making unrealistic requests; I get that this informed California policymakers' choices when they drew up this new protocol. But could we see the science, please?
This piece originally appeared in Faust's newsletter, Inside Medicineopens in a new tab or window.
"

 

[missy]

"

Picture of COVID-19 in Europe Is Complex

Infection rates are declining overall, but continuing vigilance is crucial, said WHO.

www.medscape.com

Picture of COVID-19 in Europe Is Complex​

Andrew R. Scott
January 24, 2024

"COVID is here to stay," emphasized World Health Organization (WHO) Regional Director for Europe, Hans Kluge, MD, at a press briefing on January 16, 2024. He stressed the need for continuing vigilance and efforts to keep the disease at the top of the political and healthcare agendas, while attention may be drifting to other major global events.
The WHO estimated that COVID-19 vaccines have saved at least 1.4 million lives in the WHO European Region, which encompasses 53 countries across a broad geographical area including the European Union (EU) and countries like Russia and Israel. Kluge said that at present, COVID-19 rates "remain elevated but are decreasing." However, he emphasized that the region is seeing widespread circulation of other respiratory viruses, including influenza, respiratory syncytial virus, and measles. The WHO was concerned that health services should prepare for an upsurge in the full range of respiratory virus hospitalizations in the next few weeks.
Kluge said that the unpredictable nature of the SARS-CoV-2 virus means that the emergence of new variants could cause the current situation to rapidly worsen.

A Complex Picture​

Edoardo Colzani, MD, the Principal Expert on Respiratory Viruses at the European Centre for Disease Prevention and Control (ECDC), told Medscape Medical Newsthat in the EU and European Economic Area, "Countries report a mix of increasing and decreasing trends in SARS-CoV-2 activity, COVID-19 hospitalizations, and ICU admissions and deaths, with severe outcomes predominantly among those aged 65 years and above."
The ECDC monitored the results of COVID-19 tests in selected sentinel siteschosen to give a representative sample. The percentage of positive tests in primary care sites increased from week 44 to week 49 of 2023 but fell since week 50.

Colzani said that many countries also conduct testing at non-sentinel sites, such as hospitals, schools, primary care facilities, laboratories, and nursing homes. "At the EU and EEA level, SARS-CoV-2 detections and testing in non-sentinel data were similar to those reported for sentinel data, with most countries reporting decreasing trends. However, in some countries, SARS-CoV-2 positivity and detections in non-sentinel data are notably increasing, especially in those aged 65 years and above," he explained.

Despite a decreasing trend in COVID-19 across Europe overall, data from the WHO reported an increasing trend in SARS-CoV-2 positivity in four EU reporting countries in the second week of January: Poland, Portugal, Switzerland, and Slovakia.
In terms of disease severity, Colzani said, "We wouldn't go as far as saying that there is declining severity, but surely it's not increasing...But if [vaccination] is not kept up to date, then we may see an increase in severity due to waning immunity, particularly among groups at risk."
The data available collectively from the ECDC and WHO revealed a complex picture of increasing and decreasing trends, covering rates of positive testing, hospital admissions, intensive care unit (ICU) admissions, and COVID-19–associated deaths. The values were changing significantly from week to week.

In terms of death rates, the WHO stated that although levels remained relatively low in the second week of January, Malta reported a marked increase in COVID-19 death rates in people aged 65 years and older, while 10 of the 14 countries reporting age-specific death data documented a marked decrease.

Challenges, Lessons, and Plans​

"Member States should be ready for the possible need to increase emergency department and ICU capacity, in terms of adequate staffing and bed capacity, for both adult and pediatric hospitals," said Colzani. "Hospital administrators and managers should ensure that resources, such as medical and nursing staff and equipment, are also available."
As the virus continues to evolve, the ECDC view, generally shared by the WHO, is that there are currently no new variants of concern, but there are some variants of interest that are being closely monitored. "JN.1, which is a sub-lineage of the BA.2.86 variant, has been particularly increasing in proportion recently, but without so far causing a visible impact on the epidemiological indicators," said Colzani.
The prevalence of the diverse range of issues characterized as long COVID is another major aspect of the disease. The WHO estimated that 36 million people across the WHO European region may have developed long COVID over the first 3 years of the pandemic.
Several speakers at the WHO briefing highlighted lessons learned from the pandemic to help prepare for future ones, including the importance of regional resilience, with nations and regions needing to become self-sustainable in the manufacturing of medical and other supplies and in conducting clinical trials.
Looking to the future, Catherine Smallwood, MD, COVID-19 Incident Manager of WHO/Europe, told the press briefing, "We are working…in the European region and beyond to revise and update pandemic plans [to ensure] that what we've experienced in the last pandemic can be documented and included in the pandemic plan for the next one."

Hans Kluge concluded, "…It's so important [to get] an international agreement, a pandemic accord…to tackle some issues like much quicker exchange of information, of data on clinical trials, and of sharing also the different medical countermeasures."
"

 

[missy]

"

Five Bold Predictions for Long COVID in 2024

If even one of these comes true, long COVID sufferers could enjoy some much-needed relief.

www.mdedge.com

Five Bold Predictions for Long COVID in 2024​

With a number of large-scale clinical trials underway and researchers on the hunt for new therapies, long COVID scientists are hopeful that this is the year patients — and doctors who care for them — will finally see improvements in treating their symptoms.
Here are five bold predictions — all based on encouraging research — that could happen in 2024. At the very least, they are promising signs of progress against a debilitating and frustrating disease.

#1: We’ll gain a better understanding of each long COVID phenotype​

This past year, a wide breadth of research began showing that long COVID can be defined by a number of different disease phenotypes that present a range of symptoms.

Researchers identified four clinical phenotypes: Chronic fatigue-like syndrome, headache, and memory loss; respiratory syndrome, which includes cough and difficulty breathing; chronic pain; and neurosensorial syndrome, which causes an altered sense of taste and smell.
Identifying specific diagnostic criteria for each phenotype would lead to better health outcomes for patients instead of treating them as if it were a “one-size-fits-all disease,” said Nisha Viswanathan, MD, director of the long COVID program at UCLA Health, Los Angeles, California.
Ultimately, she hopes that this year her patients will receive treatments based on the type of long COVID they’re personally experiencing, and the symptoms they have, leading to improved health outcomes and more rapid relief.
“Many new medications are focused on different pathways of long COVID, and the challenge becomes which drug is the right drug for each treatment,” said Dr. Viswanathan.

#2: Monoclonal antibodies may change the game​

We’re starting to have a better understanding that what’s been called “viral persistence” as a main cause of long COVID may potentially be treated with monoclonal antibodies. These are antibodies produced by cloning unique white blood cells to target the circulating spike proteins in the blood that hang out in viral reservoirs and cause the immune system to react as if it’s still fighting acute COVID-19.
Smaller-scale studies have already shown promising results. A January 2024 study published in The American Journal of Emergency Medicine followed three patients who completely recovered from long COVID after taking monoclonal antibodies. “Remission occurred despite dissimilar past histories, sex, age, and illness duration,” wrote the study authors.
Larger clinical trials are underway at the University of California, San Francisco, California, to test targeted monoclonal antibodies. If the results of the larger study show that monoclonal antibodies are beneficial, then it could be a game changer for a large swath of patients around the world, said David F. Putrino, PhD, who runs the long COVID clinic at Mount Sinai Health System in New York City.
“The idea is that the downstream damage caused by viral persistence will resolve itself once you wipe out the virus,” said Dr. Putrino.

#3: Paxlovid could prove effective for long COVID​

The US Food and Drug Administration granted approval for Paxlovid last May for the treatment of mild to moderate COVID-19 in adults at a high risk for severe disease. The medication is made up of two drugs packaged together. The first, nirmatrelvir, works by blocking a key enzyme required for virus replication. The second, ritonavir, is an antiviral that’s been used in patients with HIV and helps boost levels of antivirals in the body.

In a large-scale trial headed up by Dr. Putrino and his team, the oral antiviral is being studied for use in the post-viral stage in patients who test negative for acute COVID-19 but have persisting symptoms of long COVID.

Similar to monoclonal antibodies, the idea is to quell viral persistence. If patients have long COVID because they can’t clear SAR-CoV-2 from their bodies, Paxlovid could help. But unlike monoclonal antibodies that quash the virus, Paxlovid stops the virus from replicating. It’s a different mechanism with the same end goal.

It’s been a controversial treatment because it’s life-changing for some patients and ineffective for others. In addition, it can cause a range of side effects such as diarrhea, nausea, vomiting, and an impaired sense of taste. The goal of the trial is to see which patients with long COVID are most likely to benefit from the treatment.

#4: Anti-inflammatories like metformin could prove useful​

Many of the inflammatory markers persistent in patients with long COVID were similarly present in patients with autoimmune diseases like rheumatoid arthritis, according to a July 2023 study published in JAMA.

The hope is that anti-inflammatory medications may be used to reduce inflammation causing long COVID symptoms. But drugs used to treat rheumatoid arthritis like abatacept and infliximabcan also have serious side effects, including increased risk for infection, flu-like symptoms, and burning of the skin.

“Powerful anti-inflammatories can change a number of pathways in the immune system,” said Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. Anti-inflammatories hold promise but, Dr. McComsey said, “some are more toxic with many side effects, so even if they work, there’s still a question about who should take them.”

Still, other anti-inflammatories that could work don’t have as many side effects. For example, a study published in The Lancet Infectious Diseases found that the diabetes drug metformin reduced a patient’s risk for long COVID up to 40% when the drug was taken during the acute stage.

Metformin, compared to other anti-inflammatories (also known as immune modulators), is an inexpensive and widely available drug with relatively few side effects compared with other medications.

#5: Serotonin levels — and selective serotonin reuptake inhibitors (SSRIs) — may be keys to unlocking long COVID​

One of the most groundbreaking studies of the year came last November. A study published in the journal Cell found lower circulating serotonin levels in patents with long COVID than in those who did not have the condition. The study also found that the SSRI fluoxetine improved cognitive function in rat models infected with the virus.

Researchers found that the reduction in serotonin levels was partially caused by the body’s inability to absorb tryptophan, an amino acid that’s a precursor to serotonin. Overactivated blood platelets may also have played a role.

Michael Peluso, MD, an assistant research professor of infectious medicine at the UCSF School of Medicine, San Francisco, California, hopes to take the finding a step further, investigating whether increased serotonin levels in patients with long COVID will lead to improvements in symptoms.

“What we need now is a good clinical trial to see whether altering levels of serotonin in people with long COVID will lead to symptom relief,” Dr. Peluso said last month in an interview with this news organization.

If patients show an improvement in symptoms, then the next step is looking into whether SSRIs boost serotonin levels in patients and, as a result, reduce their symptoms.

"

 

[missy]

"

Long COVID Has Caused Thousands of US Deaths: New CDC Data​

Lisa Rapaport


While COVID has now claimed more than 1 million lives in the United States alone, these aren't the only fatalities caused at least in part by the virus. A small but growing number of Americans are surviving acute infections only to succumb months later to the lingering health problems caused by long COVID.

Much of the attention on long COVID has centered on the sometimes debilitating symptoms that strike people with the condition, with no formal diagnostic tests or standard treatments available, and the effect it has on quality of life. But new figures from the US Centers for Disease Control and Prevention (CDC) show that long COVID can also be deadly.

More than 5000 Americans have died from long COVID since the start of the pandemic, according to new estimates from the CDC.


This total, based on death certificate data collected by the CDC, includes a preliminary tally of 1491 long COVID deaths in 2023 in addition to 3544 fatalities previously reported from January 2020 through June 2022.
Guidance issued in 2023 on how to formally report long COVID as a cause of death on death certificates should help get a more accurate count of these fatalities going forward, said Robert Anderson, PhD, chief mortality statistician for the CDC.





"We hope that the guidance will help cause of death certifiers be more aware of the impact of long COVID and more likely to report long COVID as a cause of death when appropriate," Anderson said. "That said, we do not expect that this guidance will have a dramatic impact on the trend."

There's no standard definition or diagnostic test for long COVID. It's typically diagnosed when people have symptoms at least 3 months after an acute infection that weren't present before they got sick. As of the end of last year, about 7% of American adults had experienced long COVID at some point, the CDC estimated in September 2023.
The new death tally indicates long COVID remains a significant public health threat and is likely to grow in the years ahead, even though the pandemic may no longer be considered a global health crisis, experts said.
For example, the death certificate figures indicate:

• COVID-19 was the third leading cause of American deaths in 2020 and 2021, and the fourth leading cause of death in the United States in 2023.
• Nearly 1% of the more than one million deaths related to COVID-19 since the start of the pandemic have been attributed to long COVID, according to data released by the CDC.
• The proportion of COVID-related deaths from long COVID peaked in June 2021 at 1.2% and again in April 2022 at 3.8%, according to the CDC. Both of these peaks coincided with periods of declining fatalities from acute infections.

"I do expect that deaths associated with long COVID will make up an increasingly larger proportion of total deaths associated with COVID-19," said Mark Czeisler, PhD, a researcher at Harvard Medical School who has studied long COVID fatalities.
Months and even years after an acute infection, long COVID can contribute to serious and potentially life-threatening conditions that impact nearly every major system in the body, according to the CDC guidelines for identifying the condition on death certificates.
This means long COVID may often be listed as an underlying cause of death when people with this condition die of issues related to their heart, lungs, brain or kidneys, the CDC guidelines noted.
The risk for long COVID fatalities remains elevated for at least 6 months for people with milder acute infections and for at least 2 years in severe cases that require hospitalization, some previous research suggested.
As happens with other acute infections, certain people are more at risk for fatal case of long COVID. Age, race, and ethnicity have all been cited as risk factors by researchers who have been tracking the condition since the start of the pandemic.
Half of long COVID fatalities from July 2021 to June 2022 occurred in people aged 65 years and older, and another 23% were recorded among people aged 50-64 years old, according a report from CDC.
Long COVID death rates also varied by race and ethnicity, from a high of 14.1 cases per million among America Indian and Alaskan natives to a low of 1.5 cases per million among Asian people, the CDC found. Death rates per million were 6.7 for White individuals, 6.4 for Black people, and 4.7 for Hispanic people.
The disproportionate share of Black and Hispanic people who developed and died from severe acute infections may have left fewer survivors to develop long COVID, limiting long COVID fatalities among these groups, the CDC report concluded.
It's also possible that long COVID fatalities were undercounted in these populations because they faced challenges accessing healthcare or seeing providers who could recognize the hallmark symptoms of long COVID.

It's also difficult to distinguish between how many deaths related to the virus ultimately occur as a result of long COVID rather than acute infections. That's because it may depend on a variety of factors, including how consistently medical examiners follow the CDC guidelines, said Ziyad Al-Aly, MD, chief of research at the Veterans Affairs, St. Louis Health Care System and a senior clinical epidemiologist at Washington University in St. Louis.
"Long COVID remains massively underdiagnosed, and death in people with long COVID is misattributed to other things," Al-Aly said.
An accurate test for long COVID could help lead to a more accurate count of these fatalities, Czeisler said. Some preliminary research suggests that it might one day be possible to diagnose long COVID with a blood test.

"The timeline for such a test and the extent to which it would be widely applied is uncertain," Czeisler noted, "though that would certainly be a gamechanger."

"

 

[missy]

"

Five Bold Predictions for Long COVID in 2024​

Sara Novak
January 25, 2024

With a number of large-scale clinical trials underway and researchers on the hunt for new therapies, long COVID scientists are hopeful that this is the year patients — and doctors who care for them — will finally see improvements in treating their symptoms.
Here are five bold predictions — all based on encouraging research — that could happen in 2024. At the very least, they are promising signs of progress against a debilitating and frustrating disease.
#1: We'll gain a better understanding of each long COVID phenotype

This past year, a wide breadth of research began showing that long COVID can be defined by a number of different disease phenotypes that present a range of symptoms.
Researchers identified four clinical phenotypes: Chronic fatigue-like syndrome, headache, and memory loss; respiratory syndrome, which includes cough and difficulty breathing; chronic pain; and neurosensorial syndrome, which causes an altered sense of taste and smell.





Identifying specific diagnostic criteria for each phenotype would lead to better health outcomes for patients instead of treating them as if it were a "one-size-fits-all disease," said Nisha Viswanathan, MD, director of the long COVID program at UCLA Health, Los Angeles, California.

Ultimately, she hopes that this year her patients will receive treatments based on the type of long COVID they're personally experiencing, and the symptoms they have, leading to improved health outcomes and more rapid relief.
"Many new medications are focused on different pathways of long COVID, and the challenge becomes which drug is the right drug for each treatment," said Viswanathan.
#2: Monoclonal antibodies may change the game

We're starting to have a better understanding that what's been called "viral persistence" as a main cause of long COVID may potentially be treated with monoclonal antibodies. These are antibodies produced by cloning unique white blood cells to target the circulating spike proteins in the blood that hang out in viral reservoirs and cause the immune system to react as if it's still fighting acute COVID-19.
Smaller-scale studies have already shown promising results. A January 2024 study published in The American Journal of Emergency Medicine followed three patients who completely recovered from long COVID after taking monoclonal antibodies. "Remission occurred despite dissimilar past histories, sex, age, and illness duration," wrote the study authors.
Larger clinical trials are underway at the University of California, San Francisco, California, to test targeted monoclonal antibodies. If the results of the larger study show that monoclonal antibodies are beneficial, then it could be a game changer for a large swath of patients around the world, said David F. Putrino, PhD, who runs the long COVID clinic at Mount Sinai Health System in New York City.
"The idea is that the downstream damage caused by viral persistence will resolve itself once you wipe out the virus," said Putrino.
#3: Paxlovid could prove effective for long COVID
The US Food and Drug Administration granted approval for Paxlovid last May for the treatment of mild to moderate COVID-19 in adults at a high risk for severe disease. The medication is made up of two drugs packaged together. The first, nirmatrelvir, works by blocking a key enzyme required for virus replication. The second, ritonavir, is an antiviral that's been used in patients with HIV and helps boost levels of antivirals in the body.
In a large-scale trial headed up by Putrino and his team, the oral antiviral is being studied for use in the post-viral stage in patients who test negative for acute COVID-19 but have persisting symptoms of long COVID.
Similar to monoclonal antibodies, the idea is to quell viral persistence. If patients have long COVID because they can't clear SAR-CoV-2 from their bodies, Paxlovid could help. But unlike monoclonal antibodies that quash the virus, Paxlovid stops the virus from replicating. It's a different mechanism with the same end goal.
It's been a controversial treatment because it's life-changing for some patients and ineffective for others. In addition, it can cause a range of side effects such as diarrhea, nausea, vomiting, and an impaired sense of taste. The goal of the trial is to see which patients with long COVID are most likely to benefit from the treatment.
#4: Anti-inflammatories like metformin could prove useful
Many of the inflammatory markers persistent in patients with long COVID were similarly present in patients with autoimmune diseases like rheumatoid arthritis, according to a July 2023 study published in JAMA.
The hope is that anti-inflammatory medications may be used to reduce inflammation causing long COVID symptoms. But drugs used to treat rheumatoid arthritis like abataceptand infliximabcan also have serious side effects, including increased risk for infection, flu-like symptoms, and burning of the skin.
"Powerful anti-inflammatories can change a number of pathways in the immune system," said Grace McComsey, MD, who leads the long COVID RECOVER study at University Hospitals Health System in Cleveland, Ohio. Anti-inflammatories hold promise but, McComsey said, "some are more toxic with many side effects, so even if they work, there's still a question about who should take them."
Still, other anti-inflammatories that could work don't have as many side effects. For example, a study published in The Lancet Infectious Diseases found that the diabetes drug metformin reduced a patient's risk for long COVID up to 40% when the drug was taken during the acute stage.
Metformin, compared to other anti-inflammatories (also known as immune modulators), is an inexpensive and widely available drug with relatively few side effects compared with other medications.

#5: Serotonin levels — and selective serotonin reuptake inhibitors (SSRIs) — may be keys to unlocking long COVID
One of the most groundbreaking studies of the year came last November. A study published in the journal Cell found lower circulating serotonin levels in patents with long COVID than in those who did not have the condition. The study also found that the SSRI fluoxetine improved cognitive function in rat models infected with the virus.
Researchers found that the reduction in serotonin levels was partially caused by the body's inability to absorb tryptophan, an amino acid that's a precursor to serotonin. Overactivated blood platelets may also have played a role.

Michael Peluso, MD, an assistant research professor of infectious medicine at the UCSF School of Medicine, San Francisco, California, hopes to take the finding a step further, investigating whether increased serotonin levels in patients with long COVID will lead to improvements in symptoms.
"What we need now is a good clinical trial to see whether altering levels of serotonin in people with long COVID will lead to symptom relief," Peluso said last month in an interview with Medscape Medical News.
If patients show an improvement in symptoms, then the next step is looking into whether SSRIs boost serotonin levels in patients and, as a result, reduce their symptoms.


"

 

[monarch64]

@missy thank you for your continued vigilance and for sharing pertinent information with us. You are much appreciated!

My long covid symptom is loss of smell and taste. It has become marginally better after 2+ years of the only time I had COVID. I only experienced an uptick in my sensory perception in the past 2 months, however. I cannot positively identify any catalyst, but the one change in my general wellness routine has been the addition of B12 1000mg daily on the advice of my PCP. I began that 6 months ago after getting my lab results back--the only thing I was slightly deficient in was B12, likely because I've been vegetarian for 19 years.

The flu graphs make so much sense. My DD came down with an awful respiratory flu 2 weeks ago. It's the only time I've kept her home from school for probably 5 years--kids can't attend if they're running a fever, which she was. She was home for 2 days straight and fortunately, Friday was a snow day (yes, we don't have school or work where I live when there is significant snowfall (3-5"+) bc we aren't equipped to remove it due to it happening so rarely haha) so she had that day and the rest of the weekend to recuperate.

Again, thanks for sharing all of this, and so consistently for the past several years. I'm sure you've helped many!

 

[Daisys and Diamonds]

good news to end the month on

Stuff

www.stuff.co.nz

 

[missy]

Thanks Monnie. I hope your DD is feeling much better now. And I hope your sense of taste and smell will return in full.
Thanks Nikki for the link.

"

Respiratory Virus Surge: Diagnosing COVID-19 vs RSV, Flu​

Kelly Wairimu Davis
January 31, 2024

– Amid the current wave of winter respiratory virus cases, influenza(types A and B) leads the way with the highest number of emergency room visits, followed closely by COVID-19, thanks to the JN.1 variant, and respiratory syncytial virus (RSV). With various similarities and differences in disease presentations, how challenging is it for physician's to distinguish between, diagnose, and treat COVID-19 vs RSV and influenza?
While these three respiratory viruses often have similar presentations, you may often find that patients with COVID-19 experience more fever, dry cough, and labored breathing, according to Cyrus Munguti, MD, assistant professor of medicine at KU Medical Center and hospitalist at Wesley Medical Center, Wichita, Kansas.
"COVID-19 patients tend to have trouble breathing because the alveoli are affected and get inflammation and fluid accumulating in the lungs, and they end up having little to no oxygen," said Munguti. "When we check their vital signs, patients with COVID tend to have hypoxemia [meaning saturations are less than 88% or 90% depending on the guidelines you follow]."

Patients with RSV and influenza tend to have more upper respiratory symptoms, like runny nose, sternutation — which later can progress to a cough in the upper airways, Munguti said. Unlike with COVID-19, patients with RSV and influenza — generally until they are very sick — often do not experience hypoxemia.
Inflammation in the airways can form as a result of all three viruses. Furthermore, bacteria that live in these airways could lead to a secondary bacterial infection in the upper respiratory and lower respiratory tracts — which could then cause pneumonia, Munguti said.
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Another note: Changes in COVID-19 variants over the years have made it increasingly difficult to differentiate COVID-19 symptoms from those of RSV and influenza, according to Panagis Galiatsatos, MD, pulmonologist and associate professor at Johns Hopkins Medicine. "The Alpha through Delta variants really were a lot more lung tissue invading," Galiatsatos said. "With the COVID-19 Omicron family — its capabilities are similar to what flu and RSV have done over the years. It's more airway-invading."
It's critical to understand that diagnosing these diseases based on symptoms alone can be quite fickle, according to Galiatsatos. Objective tests, either at home or in a laboratory, are preferred. This is largely because disease presentation can depend on the host factor that the virus enters into, said Galiatsatos. For example, virus symptoms may look different for a patient with asthma and for someone with heart disease.
With children being among the most vulnerable for severe respiratory illness, testing and treatment are paramount and can be quite accurate in seasons where respiratory viruses thrive, according to Stan Spinner, MD, chief medical officer at Texas Children's Pediatrics and Urgent Care. "When individuals are tested for either of these conditions when the prevalence in the community is low, we tend to see false positive results."
Texas Children's Pediatrics and Urgent Care's 12 sites offer COVID-19 and influenza antigen tests that have results ready in around 10 minutes. RSV testing, on the other hand, is limited to around half of the Texas Children's Pediatrics and none of the urgent care locations, as the test can only be administered through a nasal swab conducted by a physician. As there is no specific treatment or therapy for RSV, the benefits of RSV testing can actually be quite low — often leading to frustrated parents regarding next steps after diagnosis.

"There are a number of respiratory viruses that may present with similar symptoms as RSV, and some of these viruses may even lead to much of the same adverse outcomes as the RSV virus," Galiatsatos said. "Consequently, our physicians need to help parents understand this and give them guidance as to when to seek medical attention for worsening symptoms."
There are two new RSV immunizations to treat certain demographics of patients, Spinner added. One is an RSV vaccine for infants under 8 months old, though there is limited supply. There is also an RSV vaccine available for pregnant women (between 32 and 36 weeks gestation) that has proven to be effective in fending off RSV infections in newborns up to 6 months old.
Physicians should remain diligent in stressing to patients that vaccinations against COVID-19 and influenza play a key role in keeping their families safe during seasons of staggering respiratory infections.
"These vaccines are extremely safe, and while they may not always prevent infection, these vaccines are extremely effective in preventing more serious consequences, such as hospitalization or death," Galiatsatos said.
"

 

[missy]

"

Patient-Centered Long COVID Research​

A Research Framework That Listens to Patients
by Sophie Putka, Enterprise & Investigative Writer, MedPage Today January 31, 2024

Two researchers from Yale are taking a non-traditional approach to studying long COVID and similar illnesses, according to the New Yorkeropens in a new tab or window: patient-centered research. In the LISTEN (Listen to Immune, Symptom and Treatment Experiences Now) trial, cardiologist Harlan Krumholz, MD, and immunologist Akiko Iwasaki, PhD, are conducting research with continuous patient input.

Krumholz and Iwasaki wrote patient participation into their trial design, and they host regular "town halls" where patients can ask questions and give feedback. Though based at Yale, the research is decentralized, meaning patients from all over the world can enroll using an app, and use online journals to write about their experience. The team expects first results from Pax-C, a phase II randomized controlled trial, in June.



The researchers believe the framework is an improvement on traditional clinical research design, which can demand time and effort from participants without much in return -- but it's not without drawbacks. Their research uses convenience sampling, and is less diverse than the NIH's RECOVER study, despite its wide criticism by patient advocates.

Patients, who are experiencing symptoms in real time, also want results that can impact their lives sooner than such research can meaningfully deliver.

"There's always that disconnect between what patients expect and what we can deliver in a timely manner," Iwasaki told the New Yorker. "I would rather be criticized for being late than put out something that's half-baked, whereas I think patients, because of their suffering -- they're really expecting something to happen much quicker."

According to the New Yorker, the same sense of urgency that propelled the AIDS movement forward, largely thanks to conflict and collaboration between government researchers and patient activists, may also apply in the search for answers on long COVID.

"

 

[Daisys and Diamonds]

Stuff

www.stuff.co.nz

it hasn't left us yet
a school is shut one day into the new year as 30 staff have covid