COVID Transmissions for 2-16-2022
Does COVID-19 destroy your T cells? Also, higher Omicron hospitalizations in kids
Greetings from an undisclosed location in my apartment. Welcome to COVID Transmissions.
It has been 792 days since the first documented human case of COVID-19. In 792, Emperor Constantine VI put his mother Irene back on the throne as co-Empress (you may remember a couple of issues ago when she was deposed). I am not sure if he let her eunuchs return from exile.
Today, a story about elevated Omicron-variant-related hospitalizations among children, and a discussion of COVID-19 impacts on T cell populations.
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Now, let’s talk COVID.
Children, especially the youngest children, are hit particularly hard by the Omicron variant
A sobering new report in Morbidity and Mortality Weekly Report (MMWR) shows that adolescents and children were about 4 times as likely to be hospitalized with the Omicron variant as they were with the Delta variant: https://www.cdc.gov/mmwr/volumes/71/wr/mm7107e4.htm
This is pretty concerning. Despite claims that the Omicron variant is inherently milder—claims which I have questioned from the beginning in this newsletter—we see an effect here that is not milder. This may be because of human behavioral changes, but the end effect is the same: more kids in the hospital.
More kids in the hospital, by the way, will be followed by more dead kids. There is no way around that. The rates of death will be lower, but I guarantee you this will not matter to the parents who lose children.
There are also concerning details in the findings as well. Currently, there is an age gap in the approved vaccination population—people under 5 years old have no vaccination options. Well, it turns out, hospitalizations in this group were 5 times as likely to be hospitalized with the Omicron variant as with the Delta variant. Please keep in mind that of course, they were not vaccinated against Delta either, so something else is going on here.
I don’t know what to say about this except that eligible children should be vaccinated and serious thought should be given to protecting young children from exposure and disease. Yes, the risk is low, but the potential for damage is high. There is an element of tragedy in any death, but the death of a child enters a new category. Kids aren’t supposed to die, and we need to treat their apparently elevated risk of severe disease with the Omicron variant as a matter of serious concern.
“T cell destruction” in COVID-19
Due to recent publications (to be discussed in a moment), I have been hearing a lot lately that COVID-19 leads to the destruction of T cell populations, and these claims have reached something of an extreme in certain circles, with claims that the phenomenon resembles HIV-mediated T cell loss.
I’m afraid that we are in a situation where the claims have outpaced the data, and I’d like to ground things a little bit. At the outset, I want to mention that this is an area of study where the scientific picture is still developing.
We have known for a long time that SARS-CoV-2 has harmful effects on the immune system, particularly in severe cases. Early in the pandemic, papers such as this one demonstrated a drop in the number of lymphocytes (white blood cells, including T cells) in patients with severe COVID-19, and proposed this drop to be a potential marker of severe disease course: https://www.nature.com/articles/s41392-020-0148-4
Since the time of these findings, there has been a worldwide effort to understand the mechanism for reduction in lymphocyte counts in severe COVID-19. This has been part of a wider effort to understand the immune dysfunctions that occur to cause severe disease.
Recently, a group of researchers applied understanding from certain HIV mechanisms to their research in SARS-CoV-2. Their data suggested that SARS-CoV-2 induces a mechanism called apoptosis to cause certain T cell populations to die.
Apoptosis is known as “programmed cell death,” because it is an orderly pathway by which cells cease their life processes and take themselves apart. Sometimes it is called “cell suicide,” but I think this uses an anthropomorphic term that adds stigma to a pretty important process.
Apoptosis is used by the body for a variety of functions. When cells develop mutations that could lead to cancer—which happens more often than most people would like to know—apoptosis destroys them. It’s when it doesn’t that cancer can develop. When cells are infected with viruses, the antiviral response can cause apoptosis to shut down an infected cell and stop it from making virus.
For immune cells, apoptosis can be involved in pruning back their populations after an infection has resolved—similarly to how a nation that has just won a war might decommission some ships afterwards. Apoptosis serves other functions in immunity as well.
These researchers knew of an apoptosis-related mechanism of T cell death in HIV, and like many scientists do, they used an experimental system set up for that finding to study whether SARS-CoV-2 could do something similar or not. They found evidence that it can: https://www.nature.com/articles/s41418-022-00936-x
Their work involved the comparison of patients hospitalized in the ICU vs not in the ICU, and demonstrated that T cell apoptosis is, in their work at least, a marker of disease severity. For example, here they demonstrated that T cells from patients in the ICU have more activated caspase-1, a protein involved in apoptosis, than non-ICU patients and healthy donors:
Now look, this isn’t actually a study that claims to be representative—and I think the variation in these samples demonstrates clearly that there is more work to be done here, but I think it is impressive that the authors identified apoptosis as a mechanism contributing to T cell death in severe COVID-19.
On the other hand, I think the overall phenomenon of T cell death in COVID-19 has been overblown and exaggerated—in a few different ways—outside of the scientific literature. I have seen it compared to HIV, a virus which kills T cells to the point where there are not enough left to defend the body from infection and people die of truly unusual illnesses that would never kill an uninfected person. If this were happening in COVID-19 patients, we would know about it. The lymphocytopenia being observed even in severe COVID-19 is not of the same nature seen with HIV infection. I think that’s important to clear up.
It is also not clear at this time if the observed lymphocytopenia has long-term consequences. So far I have not seen any uptick in other infectious diseases in people recovered from COVID-19, but it would not be the first time that a virus was known to increase the risk of subsequent infectious disease. Some viruses, like influenza, rotavirus, and RSV, are known for leading to secondary infections that follow severe cases. SARS-CoV-2 is not known for this, but perhaps that is because so far it has killed many of the people who got severe disease through its own processes. Epidemiologically, we will be studying the course and natural history of COVID-19 for quite some time.
Viruses can and do have subtler long-term effects on immunity. For example, measles virus was demonstrated (by prominent COVID-19 testing thought leader Dr. Michael Mina, no less!) to cause impacts on immunity that lead to excess infectious disease cases of various types for a couple of years after a measles outbreak: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823017/
This effect is thought to be due to depletion of B and T cells after measles infection. If there is interest, I could cover it in detail in a future “Other Viruses” column.
Anyway, it is possible that COVID-19 could do something like this after people recover. It might have been hard to detect in the initial years of the pandemic because disease control measures for COVID-19 also impacted the spread of other diseases. Or, it’s possible COVID-19 doesn’t do anything like this at all.
One thing is certain: COVID-19 causes T cells that target SARS-CoV-2 to proliferate and establish memory populations. Even though in more severe cases there are noticeable impacts on lymphocyte populations, it’s clear that in all patients who recover, T cells that respond to SARS-CoV-2 infection are generated. The T cell response to SARS-CoV-2 infection and vaccination is reviewed here: https://www.nature.com/articles/s41590-021-01122-w
Look, the bottom line is, we are still learning a lot about this disease. There may be longer-term impacts on immunity from severe COVID-19. It wouldn’t be the only virus to do something like this. From those past experiences, I would expect those effects to eventually normalize and for patients to recover. It may even happen quite quickly, which would be one possible explanation for why we haven’t seen big effects. Or it may not happen at all.
What I’m sure about is that it does not cause profound, long-term immunodeficiency like that seen with HIV. I am sure about that because we have not seen the hallmarks of such immunodeficiency in recovered COVID-19 patients.
For now I would say that it’s clear you don’t want to catch COVID-19, particularly not a severe case. To substantially reduce your risk of a severe case, get vaccinated. I do say this every issue, but it turns out to be a course of action that can help protect you from a lot of the things I end up writing about.
Part of science is identifying and correcting errors. If you find a mistake, please tell me about it.
Though I can’t correct the emailed version after it has been sent, I do update the online post of the newsletter every time a mistake is brought to my attention.
No corrections since last issue.
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And this is just one example of the type of disinfo I’ve found in that newsletter. The author makes reference to their work having been “canceled” before, so I can only assume that in the past, their work was deleted for going into a degree of extreme misinformation that was too much even for Substack.
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For length, I have left out comments from the last issue, but encourage you to go back and read the conversations on the last issue as they are often educational. There was a nice discussion about future availability of the Pfizer drug PAXLOVID in this past issue’s comments section.
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Always,
JS
"What I’m sure about is that it does not cause profound, long-term immunodeficiency like that seen with HIV. I am sure about that because we have not seen the hallmarks of such immunodeficiency in recovered COVID-19 patients."
Also, there has been a *lot* of data collected on immunity to SARS-CoV-2 itself in the recovered patients. A lot. And it does show that survivors like yourself have enhanced immunity, not reduced, to that specific virus.
Do you have any thoughts on how the widespread availability of at-home COVID tests should affect how we look at the test positivity rate? On one hand, if people are using at-home tests and then following up with PCR tests to confirm positives, this would increase the test positivity rate, and what used to be considered a "high" rate might no longer be indicative of a lot of cases that are being missed. On the other hand, the availability of at-home tests might mean that PCR tests are being skipped entirely, and we're just missing lots of cases, so we would be missing lots of cases even when the positivity rate was "low".