Covid Deranges the Immune System in Complex and Deadly Ways

Yves here. I hope the doctors and scientists in the house will pipe up. This story starts off at perhaps too non-technical a level but it quickly gets more detailed It discusses how Covid often triggers the production of autoantibodies. It’s not clear if that is an effect or a cause of more serious cases (as in how serious a culprit this is in cytokine storms). But it does appear to lead to a large range of nasty knock-on effects.

By Liz Szabo, a senior correspondent and enterprise reporter at Kaiser Health News who previously covered medicine for USA TODAY for nearly 13 years. Originally published at Kaiser Health News

There’s a reason soldiers go through basic training before heading into combat: Without careful instruction, green recruits armed with powerful weapons could be as dangerous to one another as to the enemy.

The immune system works much the same way. Immune cells, which protect the body from infections, need to be “educated” to recognize bad guys — and to hold their fire around civilians.

In some Covid patients, this education may be cut short. Scientists say unprepared immune cells appear to be responding to the coronavirus with a devastating release of chemicals, inflicting damage that may endure long after the threat has been eliminated.

“If you have a brand-new virus and the virus is winning, the immune system may go into an ‘all hands on deck’ response,” said Dr. Nina Luning Prak, co-author of a January study on Covid and the immune system. “Things that are normally kept in close check are relaxed. The body may say, ‘Who cares? Give me all you’ve got.’”

While all viruses find ways to evade the body’s defenses, a growing field of research suggests that the coronavirus unhinges the immune system more profoundly than previously realized.

Some Covid survivors have developed serious autoimmune diseases, which occur when an overactive immune system attacks the patient, rather than the virus. Doctors in Italy first noticed a pattern in March 2020, when several Covid patients developed Guillain-Barré syndrome, in which the immune systems attacks nerves throughout the body, causing muscle weakness or paralysis. As the pandemic has surged around the world, doctors have diagnosed patients with rare, immune-related bleeding disorders. Other patients have developed the opposite problem, suffering blood clots that can lead to stroke.

All these conditions can be triggered by “autoantibodies” — rogue antibodies that target the patient’s own proteins and cells.

In a report published in October, researchers even labeled the coronavirus “the autoimmune virus.”

“Covid is deranging the immune system,” said John Wherry, director of the Penn Medicine Immune Health Institute and another co-author of the January study. “Some patients, from their very first visit, seem to have an immune system in hyperdrive.”

Although doctors are researching ways to overcome immune disorders in Covid patients, new treatments will take time to develop. Scientists are still trying to understand why some immune cells become hyperactive — and why some refuse to stand down when the battle is over.

Key immune players called “helper T cells” typically help antibodies mature. If the body is invaded by a pathogen, however, these T cells can switch jobs to hunt down viruses, acting more like “killer T cells,” which destroy infected cells. When an infection is over, helper T cells usually go back to their old jobs.

In some people with severe Covid however, helper T cells don’t stand down when the infection is over, said James Heath, a professor and president of Seattle’s Institute for Systems Biology.

About 10% to 15% of hospitalized Covid patients Heath studied had high levels of these cells even after clearing the infection. By comparison, Heath found lingering helper T cells in fewer than 5% of Covid patients with less serious infections.

In affected patients, helper T cells were still looking for the enemy long after it had been eliminated. Heath is now studying whether these overzealous T cells might inflict damage that leads to chronic illness or symptoms of autoimmune disease.

“These T cells are still there months later and they’re aggressive,” Heath said. “They’re on the hunt.”

Friendly Fire

Covid appears to confuse multiple parts of the immune system.

In some patients, Covid triggers autoantibodies that target the immune system itself, leaving patients without a key defense against the coronavirus.

In October, a study published in Science led by Rockefeller University’s Jean-Laurent Casanova showed that about 10% of Covid patients become severely ill because they have antibodies against an immune system protein called interferon.

Disabling interferon is like knocking down a castle’s gate. Without these essential proteins, invading viruses can overwhelm the body and multiply wildly.

New research shows that the coronavirus may activate preexisting autoantibodies, as well as prompt the body to make new ones.

In the January study, half of the hospitalized Covid patients had autoantibodies, compared with fewer than 15% of healthy people. While some of the autoantibodies were present before patients were infected with SARS-CoV-2, others developed over the course of the illness.

Other research has produced similar findings. In a study out in December, researchers found that hospitalized Covid patients harbored a diverse array of autoantibodies.

While some patients studied had antibodies against virus-fighting interferons, others had antibodies that targeted the brain, thyroid, blood vessels, central nervous system, platelets, kidneys, heart and liver, said Dr. Aaron Ring, assistant professor of immunology at Yale School of Medicine and lead author of the December study, published online without peer review. Some patients had antibodies associated with lupus, a chronic autoimmune disorder that can cause pain and inflammation in any part of the body.

In his study, Ring and his colleagues found autoantibodies against proteins that help coordinate the immune system response. “These are the air traffic controllers,” Ring said. If these proteins are disrupted, “your immune system doesn’t work properly.”

Covid patients rife with autoantibodies tended to have the severest disease, said Ring, who said he was surprised at the level of autoantibodies in some patients. “They were comparable or even worse than lupus,” Ring said.

Although the studies are intriguing, they don’t prove that autoantibodies made people sicker, said Dr. Angela Rasmussen, a virologist affiliated with Georgetown’s Center for Global Health Science and Security. It’s possible that the autoantibodies are simply markers of serious disease.

“It’s not clear that this is linked to disease severity,” Rasmussen said.

The studies’ authors acknowledge they have many unanswered questions.

“We don’t yet know what these autoantibodies do and we don’t know if [patients] will go on to develop autoimmune disease,” said Dr. PJ Utz, a professor of immunology and rheumatology at Stanford University School of Medicine and a co-author of Luning Prak’s paper.

But recent discoveries about autoantibodies have excited the scientific community, who now wonder if rogue antibodies could explain patients’ differing responses to many other viruses. Scientists also want to know precisely how the coronavirus turns the body against itself — and how long autoantibodies remain in the blood.

‘An Unfortunate Legacy’

Scientists working round-the-clock are already beginning to unravel these mysteries.

A study published online in January, for example, found rogue antibodies in patients’ blood up to seven months after infection.

Ring said researchers would like to know if lingering autoantibodies contribute to the symptoms of “long Covid,” which afflicts one-third of Covid survivors up to nine months after infection, according to a new study in JAMA Network Open.

“Long haulers” suffer from a wide range of symptoms, including debilitating fatigue, shortness of breath, cough, chest pain and joint pain, according to the Centers for Disease Control and Prevention. Other patients experience depression, muscle pain, headaches, intermittent fevers, heart palpitations and problems with concentration and memory, known as brain fog.

Less commonly, some patients develop an inflammation of the heart muscle, abnormalities in their lung function, kidney issues, rashes, hair loss, smell and taste problems, sleep issues and anxiety.

The National Institutes of Health has announced a four-year initiative to better understand long Covid, using $1.15 billion allocated by Congress.

Ring said he’d like to study patients over time to see if specific symptoms might be explained by lingering autoantibodies.

“We need to look at the same patients a half-year later and see which antibodies they do or don’t have,” he said. If autoantibodies are to blame for long Covid, they could “represent an unfortunate legacy after the virus is gone.”

Widening the Investigation

Scientists say the coronavirus could undermine the immune system in several ways.

For example, it’s possible that immune cells become confused because some viral proteins resemble proteins found on human cells, Luning Prak said. It’s also possible that the coronavirus lurks in the body at very low levels even after patients recover from their initial infection.

“We’re still at the very beginning stages of this,” said Luning Prak, director of Penn Medicine’s Human Immunology Core Facility.

Dr. Shiv Pillai, a Harvard Medical School professor, notes that autoantibodies aren’t uncommon. Many healthy people walk around with dormant autoantibodies that never cause harm.

For reasons scientists don’t completely understand, viral infections appear able to tip the scales, triggering autoantibodies to attack, said Dr. Judith James, vice president of clinical affairs at the Oklahoma Medical Research Foundation and a co-author of Luning Prak’s study.

For example, the Epstein-Barr virus, best known for causing mononucleosis, has been linked to lupus and other autoimmune diseases. The bacteria that cause strep throat can lead to rheumatic fever, an inflammatory disease that can cause permanent heart damage. Doctors also know that influenza can trigger an autoimmune blood-clotting disorder, called thrombocytopenia.

Researchers are now investigating whether autoantibodies are involved in other illnesses — a possibility scientists rarely considered in the past.

Doctors have long wondered, for example, why a small number of people — mostly older adults — develop serious, even life-threatening reactions to the yellow fever vaccine. Three or four out of every 1 million people who receive this vaccine — made with a live, weakened virus — develop yellow fever because their immune systems don’t respond as expected, and the weakened virus multiplies and causes disease.

In a new paper in the Journal of Experimental Medicine, Rockefeller University’s Casanova has found that autoantibodies to interferon are once again to blame.

Casanova led a team that found three of the eight patients studied who experienced a dangerous vaccine reaction had autoantibodies that disabled interferon. Two other patients in the study had genes that disabled interferon.

“If you have these autoantibodies and you are vaccinated against yellow fever, you may end up in the ICU,” Casanova said.

Casanova’s lab is now investigating whether autoantibodies cause critical illness from influenza or herpes simplex virus, which can cause a rare brain inflammation called encephalitis.

Calming the Autoimmune Storm

Researchers are looking for ways to treat patients who have interferon deficiencies — a group at risk for severe Covid complications.

In a small study published in February in the Lancet Respiratory Medicine, doctors tested an injectable type of interferon — called peginterferon-lambda — in patients with early Covid infections.

People randomly assigned to receive an interferon injection were four times more likely to have cleared their infections within seven days than the placebo group. The treatment, which used a type of interferon not targeted by the autoantibodies Casanova discovered, had the most dramatic benefits in patients with the highest viral loads.

Lowering the amount of virus in a patient may help them avoid becoming seriously ill, said Dr. Jordan Feld, lead author of the 60-person study and research director at the Toronto Centre for Liver Disease in Canada. In his study, four of the placebo patients went to the emergency room because of breathing issues, compared with only one who received interferon.

“If we can bring the viral levels down quickly, they might be less infectious,” Feld said.

Feld, a liver specialist, notes that doctors have long studied this type of interferon to treat other viral infections, such as hepatitis. This type of interferon causes fewer side effects than other varieties. In the trial, those treated with interferon had similar side effects to those who received a placebo.

Doctors could potentially treat patients with a single injection with a small needle — like those used to administer insulin — in outpatient clinics, Feld said. That would make treatment much easier to administer than other therapies for Covid, which require patients to receive lengthy infusions in specialized settings.

Many questions remain. Dr. Nathan Peiffer-Smadja, a researcher at the Imperial College London, said it’s unclear whether this type of interferon does improve symptoms.

Similar studies have failed to show any benefit to treating patients with interferon, and Feld acknowledged that his results need to be confirmed in a larger study. Ideally, Feld said, he would like to test interferon in older patients to see whether it can reduce hospitalizations.

“We’d like to look at long haulers, to see if clearing the virus quickly could lead to less immune dysregulation,” Feld said. “People have said to me, ‘Do we really need new treatments now that vaccines are rolling out?’ Unfortunately, we do.”

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  1. Miami Mitch

    Wasn’t there some woman on here talking about this a while ago? How it is more the immune system reaction that kills rather than the virus itself? I thought it was interesting but she received a lot of push back. Is there anyway to search the comments? I would like to see if my memory is still workin’.

    1. Jason

      Krystyn was pursuing this line of inquiry. It goes against essentially everything established medical practice is based on. More significantly, it’s completely foreign to most people’s underlying assumptions about things. Thus the pushback, even from people normally very open to different ideas. The ideas they’re open to are always safely contained within the same framework. This is an entirely different framework to operate in. Very difficult.

    2. lyman alpha blob

      I think the term used at the time was ‘cytokine storm’. That term isn’t used in the article but I believe it’s the same phenomenon as described above. You might try putting that into the search tool underneath our snow leopard friends.

    3. CoryP

      Just for the record Krystyn (a form of the name Christian) Podgajski is a guy.

      He was a big proponent of zinc at the beginning and I think that was somewhat out of the mainstream.

      As far as I remember, the idea that the immune system causes the majority of damage during COVID was never regarded as crazy by the medical establishment. Cytokine storms have been a thing for a long time.

      But I could just be misremembering. I’m sure he did get pushback on some stuff— I had some (unspoken) issues myself with his interpretation of biochemical studies leading to firm conclusions about macro scale illness. But he has been vindicated in most if not all of what he said.

      Anyway I hope he’s okay too!

      He has a Twitter account that I’m currently attempting to re-find. And I do think he commented within the last 6 months after a long period of silence. Googling now.

    4. NCdoc

      Physician here. Most people don’t realize that a lot of (sometime the most) damage that happens in an infection occurs due to the immune system’s reaction and less so the pathogen. This is not uncommon in viral illnesses. The immune system uses highly reactive free-radical oxygen/peroxides to chemically destroy targets. Our organic molecules are just as vulnerable to this oxidation as the pathogen’s though. If the immune system acutely is very active, and there is little protection to this oxidation in your own tissue, your own tissue will be destroyed — and if the immune reaction becomes a storm throughout the body, you can have multi organ injury/failure from this. This is why antioxidants (chemicals found abundantly in various plants) are so important to health. Plant based nutrition has millions of benefits – this is one of them (much better than supplements). One large subset of severely ill covid patients are those who start off with a cold — then after days time, rapidly deteriorate into acute lung injury and respiratory failure. This is an example of the physiology described earlier — and is more common in those people who were obese, elderly, and less healthy (on dialysis, advanced dementia…) — all with poor nutrition. This is why the hypotheses about zinc, vitamin C, hydroxychloroquine, vitamin D has merit — as it could possibly diminish the storm of inflammatory injury and decrease the severe lung injury. The media and the medical community got quickly distracted with studies done on ICU patients who had already succumbed to acute lung injury and therefore unfortunately did not pursue a more important question about whether those interventions could prevent the acute lung injury to begin with. Understand that what I have described is relevant to Miami Mitch’s post and not to the article. The idea of cross reactivity between foreign epitopes and your own epitopes is important in trying to understand autoimmune illness — and partly why there should be caution around any vaccine — which by definition challenges your immune system and body with foreign epitopes.

      1. Miami Mitch

        I was wondering why people have a worse reaction with the second shot, and why there is so much difference.

        I have read things like “That’s because the second dose is amplifying the lessons of the first dose, which taught your body how to recognize the coronavirus as an enemy, Poland explained.”

        But it does not make intuitive sense. Why is there no immune reaction at the first dose? And what about all the people who have no side effects from the second shot? Based on what mr poland said above, does that mean it did not work? Do the people who have a bad second shot reaction actually have some of these deficiencies or poor nutrition? I do not like how they gloss over this.

        I am trying to “follow the science”.

        Well I get my first shot around the 24th so we will see.

      2. Lorna Johnson

        ‘The immune system uses highly reactive free-radical oxygen/peroxides to chemically destroy targets’…What about the role of electromagnetic radiation in ‘helping’ to increase the free-radicals? There are so many papers published on ‘reactive oxygen species’ and electromagnetic radiation…

  2. Terry Flynn

    This both scares me but also is going to be my printout when I see the dermatologist. I’ve been referred for auto-immune condition causing sudden hair loss following unexplained skin lesion. This began soon after suspected covid-19 infection a year ago and has not settled.

    I’ve also been to ER when I got an unexplained ruptured vein. I didn’t even bother talking to the GP about my brand new rheumatoid arthritis symptoms which also appeared soon after March 2020. I won’t bore people with the other symptoms I’ve had for almost a year but suffice to say this time I’m demanding more tests and referral to immunologist too if necessary.

    1. john_brewster

      I am sorry to hear of your symptoms.

      It has been known for decades that people with certain HLA antigens are at risk for auto-immune diseases triggered by a viral infection. The natural role of HLA-B27 is to bind viruses for presentation to the immune system’s T and B cells.

      HLA-B27 binds and presents peptides from influenza, HIV, Epstein-Barr virus, and other viruses. This leads to vigorous and specific cytotoxic T lymphocyte responses, which play an important role in the body’s immune response to these viruses. HLA-B27 thus carries out its natural function highly effectively. Although many theories have been proposed to explain the role of HLA-B27 in the pathogenesis of spondyloarthropathy, we favour those postulating that the pathogenic role of HLA-B27 stems from its natural function. For example, the ‘arthritogenic’ peptide hypothesis suggests that disease results from the ability of HLA-B27 to bind a unique peptide or a set of antigenic peptides.

      HLA-B27: natural function and pathogenic role in spondyloarthritis

      However, HLA-B27 is strongly associated with “reactive” (i.e., autoimmune) spondylitis

      HLA-B27 strongly correlates with certain autoimmune diseases, such as [R]:
      • Psoriasis
      • Ankylosing spondylitis (spine deformation)
      • IBD (inflammatory bowel disease), in combination with spondylitis
      • Reactive arthritis (Reiter’s syndrome)—inflammation of the joints, urethra, and eyes

      These conditions fall under the umbrella of spondyloarthritis, with the most common form being ankylosing spondylitis (AS). In AS, inflammation gradually fuses the vertebrae in the spine, causing back pain and limited movement. It usually affects young men [R, R].

      The connection between HLA-B27 and ankylosing spondylitis (AS) is extremely strong: 90–95% of all AS patients have this gene. For other autoimmune conditions, the prevalence of HLA-B27 ranges between 50-90% [R].

      Does this mean almost everyone with HLA-B27 will get AS or another autoimmune disease? Not at all!

      A solid body of evidence also implicates the role of microbes in autoimmune disorders associated with HLA-B27 [R, R, R].

      Microbial infections such as Salmonella, Yersinia, Klebsiella, and Chlamydia can contribute to autoimmune disorders in HLA-B27 carriers because [R, R, R, R, R, R]:

      1. They increase the expression of HLA-B27 on the surface of infected cells.
      2. Some parts of the HLA-B27 antigen are similar to peptides from these bacteria, so the immune system attacks them.
      3. This antigen weakens the anti-bacterial immune response, leading to persistent infections that trigger autoimmunity.

      A Key Genetic Player in Autoimmunity (HLA-B)

      1. Terry Flynn

        Many thanks. I’m PhD (med stats) not medical doc but I know who to ask to understand things that go beyond my paygrade. Ironically I used to work with top genetic epidemiologists and clinicians doing work looking at genes. Whaddya know, within 2 minutes of beginning to follow up references to HLA-B27 I was led not only to another condition I have had but to recent papers by a clinician who treated me / worked in my dept. (This clinician liked my seminars and asked good questions so probably remembers me even though we’re going back to around 2008.)

        1. john_brewster

          You are welcome.

          Whenever I hand out links to medical papers, I worry that I am going to mislead non-scientists. I feel better knowing that you are a medically knowledgable, and that the link was on-target.

    2. Marduk

      Perhaps you’ve already done so, but you don’t explicitly say… I would consider asking your GP for a referral to a rheumatologist. My wife is a rheumatologist and has seen countless new patients with no personal or family history of rheumatologic/autoimmune disease spontaneously crop up after a bout of COVID. While a rheumatologist can’t cure what ails you, per se (I’m not aware of any medical “cure” for autoimmune disease), they can at least manage and alleviate your symptoms — or in a best case scenario, put the disease in remission.

      As for whether these new post-COVID autoimmune cases are permanent or temporary afflictions, I don’t think anyone knows yet. Perhaps there are physicians in the comments who are up to date on recent literature (or can correct my layman’s characterization of what rheumatologists do if I’ve inadvertently misinformed).

  3. Dean

    I think this is an overall good review of the immune system changes coronavirus can cause. It should be noted that this is not limited to coronavirus. Other viral and bacterial infections (and even vaccines) can lead to autoimmune antibody and/or killer cell reactions. Antigenic mimicry (thought to be the cause of rheumatic fever) is one possible mechanism.

    My only concern is this statement:

    “Key immune players called “helper T cells” typically help antibodies mature. If the body is invaded by a pathogen, however, these T cells can switch jobs to hunt down viruses, acting more like “killer T cells,” which destroy infected cells. When an infection is over, helper T cells usually go back to their old jobs.”

    I have never heard of T helper cells functioning as killer cells. They just don’t have the molecular machinery need to recognize and kill infected cells. Perhaps the statement meant that T helper cells become TH1 cells which secrete specific cytokines that drive killer CD8 and NK cells.

    1. Chris#5

      You are basically right, this was put rather clumsily in the article. Firstly, the kind of CD4 (helper) cells that assist antibody production are largely “T follicular-helper”, rather than “T helper 1” or “T helper 2” (TH1, TH2) cells. TH1 and TH2 cells, as you mention, make cytokines that could damage other cells directly. Further, (1) CD4 T cells are pretty plastic (ie, daughter cells can potentially change functionally depending on their milieu) and (2) the existence of autoantibodies to a protein says there was a CD4 T cell that recognised that protein (“linked recognition”). So, in addition to the problem mentioned in the article (autoantibody targeting of protein, for example interferon), there is the added possibility of CD4 T cells recognising self proteins causing direct autoimmune damage.
      There, got some use for my last couple of grant application introductions in this comment! To your other point, however: at least in vitro, CD4 T cells can be killers! My old lab worked on that quite a bit a couple of decades ago.

      1. Dean

        Thanks for your response that CD4 T cells can be killers! I had been rethinking this issue. The article seemed to imply that CD4 cells could convert to CD 8 or Natural killer cells (or perhaps I just inferred this). I had forgotten that CD 4 cells can kill through Fas:Fas ligand or potentially TNF mechanisms.

        I hope your grant applications were successful.

  4. SKM

    Thanks so much for posting this article. It brings together really well what is known and/or guessed at about the key role played by the immune system in making this disease so serious, and not only for the clearly seriously ill. It clarifies for me what is known and what isn`t so far but shows where research needs to concentrate (and how revealing this all is for infectious disease course generally) – this disease so far has made even immunologists realise how much about the immune system is still a mystery. Great article, again thanks!!

  5. Juneau

    Back in the spring I saw a video by a Howard Hughes Medical Institute scientist who predicted autoimmunity from this virus. The reasoning goes like this: Covid is a big virus, and when the body destroys it, it breaks into many many parts. Some of these parts, just randomly, may resemble human molecules, so in the body’s efforts to get rid of Covid it may learn to go after human molecules that look the same. He claimed that this had already been studied and there were many homologous parts to cause this kind of reaction. I am trying to find the video from the youtube channel Howard Hughes Medical Institute.

  6. PlutoniumKun

    For those interested, there is a very interesting 2 hour conversation here between Dr. Roger Seheult and Dr. Rhonda Patrick on treating covid – they are a good mix as Patrick comes from the nutrition/research side of things while Dr. Seheult is more a ‘hands on’ physician. There are timestamps beneath it for those who want to see specific parts of the conversation of interest. Some of the things they discuss – like Vitamin D – might be of interest to those who want to make their own personal decisions when it comes to reducing personal risk.

    1. PlutoniumKun

      Just to add to this – at the very end they discuss their personal approaches to reducing vulnerability to Covid. In summary it involves boosting your immune system by making sure you get a good sleep every night, take hot and cold showers alternatively, take Vitamin D and zinc supplements, eat lots of natural anti-oxidant foods and (slightly more controversially), take the supplement NAC (N-Acetyl Cysteine).

      1. bulfinch

        Dr. Rhonda Patrick has some very interesting theories on health; however, I became a bit more cautious upon discovering she was an acolyte of Dr. William D. Kelley, the former Texas dentist who went on to fame as the laetrile-and-coffee-enemas-as-cancer-treatment-guy back in the late 70’s.

        1. PlutoniumKun

          I’ve not heard of that connection and a quick google doesn’t show any link. I’d be interested to hear if you have any evidence for that supposed link.

        2. Christopher D Pinkleton

          I am taking zinc, D, C and K supplements at the moment, but I am still skeptical about “antioxidants as miracle immune boosters” narrative that dates back about 50 years.

          Remember when vitC prevented the common cold and cancer? (It does neither in high doses compared with adequate nutrition.)

          I used to be on the antioxidants for immortality train myself, with megabytes of C and the like. NAC was on my daily program for quite a while.

          Problem is, most of the hypothesises behind mega-doses of vitamins turned out to be completely false. You can’t prevent aging by taking megadoses of antioxidants, and mega-vitamin takers get sick just as often as everyone else. I doubt I did much during my megadosing years beyond accelerate kidney stone formation (C ain’t completely harmless) and boost my cancer risks. (E is particularly bad for prostate cancer, for example)

          So I’m skeptical about folks boosting vitamins that were touted as “miracle life extenders ” now being boosted as super immune boosters, now with a different scientific rationale—but the same economic rationale insofar as they make big money for the same old supplement sellers.

          I’m waiting for the claim that IV chelation cures Covid, can’t be far off…

    2. NCdoc

      One of the many things that make me upset about the media hysteria about covid is that there has been neglect to share this type of info — which is real!! I am a physician who has cared for lots of covid patients in the hospital. Yes, wash hands and don’t leave home if you are sick — but just as important: eat lots of plants (with a variety of colors), get good sleep, get physical fitness, and if you are overweight, lose weight. These things are associated with not only reduction of morbidity/mortality from covid, but from morbidity and mortality from most everything else.

      1. marku52

        Get your Vit D measured. Low Vit D is quite dangerous with this disease, and the US RDAs are absurdly low. Obviously POC are more prone to deficiency (IIRC about 80% of African Americans are deficient, Latins not quite as much. And of course the winter months in the higher latitudes promote deficiency as well. There is evidence that this is one of the reasons for the flu season being in the winter.

        Also obesity ties into D deficiency, and consuming HFCs also destroys Vit D. A multiple whammy for poor black people with low income diets.–Who do seem to be disproportionately damaged by Covid.

        1. marku52

          Oh Yeah, Fauci takes 6000IU per day. But doesn’t bother to recommend anyone else do it.

          1. Baldanders

            I posted a long comment on my own comment on vitamins and covid, but the moderation ate it. :(

            In short: I’m taking Zinc, C, D, and K now, but as a former megasupplimenter, I am skeptical about vitamins that were once touted as longevity boosters (based on the flawed “more antioxidants = less aging” idea) are now going to save us from covid.

            Remember when lots of C would prevent colds and cancer? Whoops.

  7. Yikes

    So… Celiac here, with some other autoimmune issues including thyroid. I’ve dodged the virus so far, but I’m concerned about the effects of vaccination and of eventual exposure in the wild with my existing conditions. Haven’t found much so far on covid and/or vax issues for autoimmune people… anyone out there have any info?

    1. Lee

      FWIW, my ME/CFS specialist advised me to get vaccinated. I got the first Pfizer shot three days ago. So far, so good.

    2. Ella

      I have hashimoto’s and am curious too. Brief search online tells me it’s not an issue as , say, diabetes.

    3. Marduk

      My wife is a rheumatologist and also has quite serious autoimmune disease herself. She chose to get vaccinated (Moderna) in January (early access as a healthcare worker) and has had no adverse reaction other than a little fatigue for a day or two after the second dose. She is also recommending to her patients that they get vaccinated. She has done her best to keep up on the literature and discusses COVID on a daily basis with many of her rheumatology and general practice colleagues. While she acknowledges and explains to her patients that there is almost no hard data regarding adverse effects on patients with autoimmune disease, she is increasingly convinced, especially with passage of time and reading and maintaining dialogue with colleagues, that “the benefits of vaccination for autoimmune patients with compromised immune systems outweigh the risk of adverse reaction” (I’m quoting her on that last bit). I’m also not aware of any of her patients having adverse reactions to the vaccine (we talk about all things COVID daily so I think she would mention it, but obviously this is not good evidence of the vaccines’ safety).

      Of course, do your own homework and speak with as many physicians as you need to to feel comfortable before getting vaccinated. I’m just a layman relaying my wife’s personal experience and what I understand to be her medical opinion about the vaccines’ safety. Some rheumatologists or other practitioners may have a different opinion. I can’t say I know that there is a firm consensus yet.

    4. Anonymous 2

      COVID Zoe in the UK have just done a webinar which covered COVID and people with immune system problems. It might be helpful to you to look for that on YouTube.

    5. Yikes

      Thanks again so much for all the responses!

      Just to be clear, I’m very pro-vax, and I think in this case I will have to get vaccinated regardless of side effects… no way out but through in a pandemic. But I’d still like to know what to prepare for, and I also don’t know if any of the particular brands might be better than others in this specific situation. I have to say it’s all worrying me a lot, especially with this talk about about IgG issues.
      Last time I asked my specialist at a major research hospital, he said all the gastro autoimmune people have gone to ground for the moment and he has no feel for outcomes yet.

  8. cojo

    It’s nice to see this article linking viral infections to autoimmune disease. Our immune system is almost as complex as consciousness/life itself. Add to this the interplay of environmental factors and… you get the picture. I recall during medical school the alien nature of autoimmune diseases due to their genetic links, ability to affect multiple, random, organ systems, as well as to the unknown (always “some” virus or other random environmental) triggers. They have been linked to everything from Alzheimer’s, Type I diabetes, coronary artery disease, and even schizophrenia. When a novel infectious vector rips through a susceptible (in the immunological sense) population you will see all kinds of mysterious and unexpected clinical outcomes. What is often forgotten about COVID 19 is that the great majority of cases are treated as outpatients with relatively benign courses and no significant long term sequelae. However, the 20% or so cases that are not so lucky end up with the more frightening variety of clinical outcomes. We are now figuring out what causes a worse clinical course. Factors such as the diverse genetic make up of individual immunity (see John Brewster’s review of HLA components), environmental factors (pollution, climate, sunlight/vitamin D levels) and individual co-morbidities (age, smoking history, diabetes, obesity, poor microbiome diversity, etc) are now being teased out. Scientists will be dissecting the mountains of data from this pandemic for decades!

    1. NCdoc

      I like your 2nd sentence. I’ve been a hospitalist for almost 20 years — and as the years go by, I feel less and less confident in mankind’s understanding of nature — and have developed a healthy amount of humility and appreciation for life/nature/universe/God. Given the exponential activation cascades which can be diverted at any level, and the tenuous buffering between the “on” and “off” states, I’ve always felt like the immune system and the coagulation systems were the most complicated and hard-to-predict systems in the body. With a head in mathematics, I used to think in medical school that it is impossible to predict the outcome of those systems when trying to intervene in the cascades (like trying to use a paddle to intervene in the outcomes of ocean waves) — and over time feel like humans will never be able to reliably affect either of those systems. A good example of this is all of the autoimmune illnesses created by the newer immune modifying cancer treatments.

      1. john_brewster

        Given the exponential activation cascades which can be diverted at any level, and the tenuous buffering between the “on” and “off” states, I’ve always felt like the immune system and the coagulation systems were the most complicated and hard-to-predict systems in the body. With a head in mathematics,…

        When I worked in drug discovery, I acquied the same skepticism towards simple fixes. Biology is like the internet, it routes around damage (or drug interventions). You had to find a real chokepoint in the cascade that could not be routed around. One time we thought we had a fantastic cancer drug, until they tested it in dogs. The dogs went blind, because the critical pathway for cancer was also a critical pathway for retinal metabolism.

        You say you are of a mathematical bent. It may interest you to know that the immune system has been proven to behave as a “sparse distributed memory”. See Immunological memory is associative There is a branch of AI called artificial immune systems that is used in – wait for it – in computer virus research.

        1. john_brewster

          So the SDM paper is actually referenced by current day Covid researchers, in the context of antibody dependent enhancement.

          It is actually typical for the immune system to respond, to what it already knows, a phenomenon that has been observed in many infections with closely related viruses and has been termed “original antigenic sin.” The question then arises whether such cross-reactive antibodies are protective or not against the new virus. The worst scenario would be when such cross-reactive memory antibodies to related coronaviruses would not only be non-protective but even enhance infection and the clinical course. Such a phenomenon of antibody dependent enhancement (ADE) has already been described in several viral infections. Thus, the development of IgG against SARS-CoV-2 in the course of COVID-19 might not be a simple sign of viral clearance and developing protection against the virus. On the contrary, due to cross-reaction to related coronavirus strains from earlier infections, in certain patients IgG might enhance clinical progression due to ADE. The patient’s viral history of coronavirus infection might be crucial to the development of the current infection with SARS-CoV-2. Furthermore, it poses a note of caution when treating COVID-19 patients with convalescent sera.

          Antibody Dependent Enhancement Due to Original Antigenic Sin and the Development of SARS

          Being aware of ADE, I have been reluctant to go for the mRNA treatment. Even the genuine vaccines (J&J, AZ) have not collected enough data to understand the risk pattern.

          Is anyone working up HLA profiles of the severe cases of covid and ADE responses? It would seem a logical thing to do, and their seems to be infinite resources for vaccines. But the WHO isn’t even following through on their earlier trial effort.

          WHOs treatment megatrial is at a standstill

          The only global trial of potential COVID-19 treatments is languishing. The World Health Organization’s (WHO’s) Solidarity trial, set up last year to quickly test potential COVID-19 therapies with tens of thousands of patients, produced headlines in October 2020 when it showed that four candidate treatments offer little benefit. But since then, it hasn’t launched any new tests. On 27 January, John-Arne Røttingen, who works at Norway’s foreign ministry and chairs the trial’s executive group, pulled the plug on the study’s only remaining arm, which tested the antiviral remdesivir. “The Solidarity trial is now on pause,” he says.

          Science 05 Mar 2021:
          Vol. 371, Issue 6533, pp. 972-973
          DOI: 10.1126/science.371.6533.972

      2. cojo

        The immune system and the coagulation system are closely related. Many of the functions of platelets, as studied in horseshoe crabs, are integral to the immune response to bacterial infections. Hence why one sees with increased thrombotic events in certain types of infections with gram negative organisms or viral infections (COVID, influenza).

        I think an important factor for both these systems is homeostasis, or a fancy medical term for balance. When your immune system gets out of balance you get pathology, cancer and increased infections on the one end (weak immune system) and acute and chronic inflammatory disorders (hyperactive immune system) on the other end. The key is figuring out on which side of the spectrum you are on and trying to help correct it. Many of the therapies around are there to just tip the scales, think of many antibiotics that don’t necessarily kill the pathogen but inhibit growth just enough for your own immune system to finish the job.

  9. Susan the other

    Thanks for this link. It was really interesting. Mostly because the panic over mRNA vaxes having the potential to trigger auto-immune disorders. It’s good to know that viruses have long been known to do the same. So certainly it’s 6s whether you get Covid or the vaccine – in terms of an unwanted autoimmune response. I was thinking it’s riskier to get the shot because of the nano-lipids and easier cell invasion than it is to catch the real thing. Anyway, I’m pretty sure I’ve had Covid twice. Last March – a killer intestinal flu, but only lasted about a week. And again when the new strains started showing up in November which was not bad, but had some of the weird characteristics of the first bout. So anyway… I’m still planning to get the Johnson. I think with my autoimmune disorders I don’t need anything as high-powered as an mRNA vaccine. I’ll stick with a good, old-fashioned dead virus.

    1. Marduk

      See my response to “Yikes” above regarding my wife’s personal experience with the Moderna vaccine (she has serious autoimmune disease and experienced no adverse reaction other than mild fatigue after the second dose), as well as her opinion as a rheumatologist about the vaccines’ safety.

      TL;DR: she recommends people with autoimmune disease get vaccinated, but by all means, do your homework and consult your own physician.

    2. Stephen Gardner

      I think it might be misleading to say J&J is a live virus vaccine. As I understand it, it’s a repurposed cold virus that causes your cells to make the spike proteins for covid. It does not replicate itself. When it gets into your cells it uses the cell machinery to manufacture proteins not copies of itself.

    3. Fern

      Like Cuibono and Stephen pointed out, Johnson & Johnson isn’t an old-fashioned inactivated or attenuated virus vaccine. It’s a viral-vector vaccine, which is also a very new technology. Like the mRNA vaccines, it hijacks a few of our own cells to assemble the coronavirus spike proteins that are recognized by your immune system, but it uses a different mechanism to slip the instructions into the cell.

      To make this vaccine, they inactivate an adenovirus, insert man-made genetic instructions into the adenovirus genome, and use the inactivated adenovirus to slip the man-made genetic instructions into your cell, rather than using a lipid envelop to slip the genetic instructions into your cell as the mRNA viruses do. I believe that the Novavax vaccine which is currently being evaluated does not require the hijacking of your cells, but rather uses moth cells to create the spike protein.

      The Chinese have vaccines that use the more old-fashioned approach you’re referring to, using simple inactivated viruses.

  10. JEHR

    We are fortunate to have so many intelligent commenters on NC. I have thoroughly enjoyed them all on this topic which is, to me, very complicated.

  11. Gregory Etchason

    Mortality in infectious disease is generally a result of the immune response not the pathogen per se. Your immune system can save you, leave you chronically ill or take you away. Most conditions in the subspecialty of Rheumatology are a likely manifestations of genetic predisposition and viral illness. Many chronic disorders are linked to prior infections. Blockage in the carotid arteries are associated with antibody to the Chlamydial bacteria in 90% of samples.

  12. John Emerson

    Just a sidelight: the inflammation resulting from mosquito bites is also an immune reaction and not the result of the bite, and after enough bites the immune system decides that mosquitos are normal and turns off. I’ve been part of two natural experiments on this, when the Minnesotans didn’t notice any problem but our friends from elsewhere were miserable and ended up covered with bumps.

  13. Jeremy Grimm

    After reading this post and the many learned comments regarding different Corona autoimmune responses plausibly explaining “long Corona” [not to slur Corvidae] — I sincerely hope some portion of the $1.15 billion Congress allocated to the National Institutes of Health will sponsor basic research of the immune system in addition to statistical studies of long Corona sufferers and the varieties of symptoms they suffer.

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