Misinformation About Natural COVID Immunity: Part 1

by Robert Nelson, MD

Misinformation #1

Mild COVID cases result in short-lived or weaker immunity

It is not uncommon in discussions pertaining to COVID immunity to read or hear speculation that the severity of COVID illness may have a bearing on future immunity to SARS-CoV-2; the caution being that mild or asymptomatic infections might result in weaker or less durable immune responses.

This sounds logical on the surface when we consider commonly held maxims about stresses applied to systems. For example, “what doesn’t kill us, makes us stronger” or “No pain – no gain” or “the strongest steel is forged in the hottest fire.”

The broader concept being that stress on a system makes that system stronger or more resilient. But analogies based on metaphors eventually break down due to a tendency to over-simplify complex systems, such as in human immunity.

Ali Ellebedy, Ph.D. of the Department of Pathology and Immunology, Center for Vaccines and Immunity to Microbial Pathogens at Washington University School of Medicine, St Louis, MO had this to say on the topic in a May 2021 article in EurekAlert:

“Last fall, there were reports that antibodies wane quickly after infection with the virus that causes COVID-19, and mainstream media interpreted that to mean that immunity was not long-lived. But that’s a misinterpretation of the data. It’s normal for antibody levels to go down after acute infection, but they don’t go down to zero; they plateau. Here, we found antibody-producing cells in people 11 months after first symptoms. These cells will live and produce antibodies for the rest of people’s lives. That’s strong evidence for long-lasting immunity.”

“People with mild cases of COVID-19 clear the virus from their bodies two to three weeks after infection, so there would be no virus driving an active immune response seven or 11 months after infection. These cells are not dividing. They are quiescent, just sitting in the bone marrow and secreting antibodies. They have been doing that ever since the infection resolved, and they will continue doing that indefinitely.”

In the same study co-authored by Professor Ellebedy, fellow author Jackson Turner, Ph.D. had this to say when discussing the issue of mild vs severe illness and its effect on the immune system:

“It could go either way, inflammation plays a major role in severe COVID-19, and too much inflammation can lead to defective immune responses. But on the other hand, the reason why people get really sick is often because they have a lot of virus in their bodies and having a lot of virus around can lead to a good immune response. So, it’s not clear. We need to replicate the study in people with moderate to severe infections to understand whether they are likely to be protected from reinfection.”

The main conclusions of their study are summarized here:

“Anti-S antibody titres correlated with the frequency of S[pike]-specific plasma cells in bone marrow aspirates from 18 individuals who had recovered from COVID-19 at 7 to 8 months after infection. S-specific BMPCs were not detected in aspirates from 11 healthy individuals with no history of SARS-CoV-2 infection. We show that S-binding BMPCs are quiescent, which suggests that they are part of a stable compartment. Consistently, circulating resting memory B cells directed against SARS-CoV-2 S were detected in the convalescent individuals. Overall, our results indicate that mild infection with SARS-CoV-2 induces robust antigen-specific, long-lived humoral immune memory in humans.”

This same group from Washington University is now studying whether vaccination also induces long-lived antibody-producing cells.

But maybe we’ve got it backwards. Instead of a severe infection yielding future protection, what if it reflects a weakness or derangement in the immune response? Could it be that the reason some people have mild cases of COVID-19 is BECAUSE their immune systems are working better? This so-called adaptive immune response may also help suppress the mediators of inflammation implicated in severe lung disease often associated with fatal cases of COVID-19. Or is there some dysfunction or exaggerated responses or missing elements that cause some to have more severe symptoms?

This from an article in Verywell Health.

The April study, which was published in the journal Nature Medicine, found higher levels of certain immune cells in people with COVID-19 who did not have symptoms. Researchers also found that people who had more serious forms of COVID-19 did not have elevated levels of these protective immune cells, and also gained inflammatory cells.1

figure5In people with asymptomatic cases, the researchers found increased levels of B cells, which produce antibodies that are found in mucus passages like the nose. These cells are thought to be protective against COVID-19. But those same cells were missing in people with severe cases, suggesting that this function of the immune response failed.

This, the researchers say, could help explain why people with severe forms of COVID-19 are at risk of developing lung inflammation and blood clots.



And finally, another study shows that all post-infection participants, even asymptomatic recoverees, displayed Receptor Binding Domain-specific Memory B-cells to the Variant of concern for at least 12 months.

“In contrast to plasma Ab titers, SARS-CoV-2 S1 and RBD specific MBCs were present above the limit of detection in all subjects in this analysis, even asymptomatic subjects. Moreover, SARS-CoV-2 S1 and RBD-specific MBCs remained detectable for as long as 11.75 months post-infection.”

This finding, that VoC-RBD-reactive MBCs are present in the peripheral blood of all (24) subjects including those that experienced asymptomatic or mild disease, provides a reason for optimism regarding the capacity of vaccination, prior infection, and/or both, to limit disease severity and transmission of variants of concern as they continue to arise and circulate.”

It’s safe to say that the COVID-19 virus doesn’t decide to take it easy on some and hit others harder. It does not discriminate.

So, based on the data presented it’s reasonable to conclude that having a mild or asymptomatic case of COVID-19 is more likely an indicator of a robust immune response, rather than simply a function of a smaller viral inoculum or a fortunate random event. And contrary to some speculation in the media about decaying natural immunity, the components that protect over the long-term (cellular immunity) persist long after antibody levels fall to plateau. And evidence exists that robust and durable immune responses accompany even the mildest cases of COVID, but without the devastating effects of uncontrolled inflammation.

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