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For clarity, here is a summary of my question, per anongoodnurse's comment:

Does a lower peripheral lymphocyte count resulting from recent immunization render us more susceptible to infection by other viruses?


There are many bad-faith arguments circulating that suggest COVID-19 vaccines are doing more harm than good. One talking point is that COVID-19 vaccination leads to a temporary reduction in circulating white blood cells, leaving vaccinated individuals susceptible to infections in the short term. Former NYT reporter Alex Berenson has been making such claims on Twitter:

1/ The fact the mRNA vaccines transiently suppress lymphocytes after vaccination has come up repeatedly on the feed as a possible explanation for post-vaccination deaths. Fact check: This is TRUE. @BioNTech_Group acknowledged it its papers (both 162b1 and 162b2 did so)

2/ By the way, they also lead to a sharp rise in C-reactive protein. Would love immunologists or virologists to chime in on whether these changes may be in any way clinically meaningful

As sources, Berenson cites two papers detailing the results of phase I/II trials for mRNA vaccine candidates.1,2

Derek Thompson addresses this Tweet and other claims made by Berenson in an article in The Atlantic 3, in which Thompson asks experts to challenge the misinformation shared by Berenson. Regarding the Tweet above, virologist Shane Crotty said the following:

The claim he is making is simply fearmongering, connecting a simple physiological event with bogus claims of deaths ... The observation of lymphocyte numbers temporarily dropping in blood is actually a common phenomenon in immune responses ... The cells are not gone. They come back to the blood in a few days. It is generally a good sign of an immune response, not the opposite.

While Berenson's claims regarding post-vaccination deaths are derived from his (willful?) misinterpretation of the data, Crotty's response got me thinking about the immunological dynamics of vaccination. My question: Does the localization of lymphocytes to secondary lymphoid tissues lead to reduced circulating lymphocytes and a subsequent increase in susceptibility to secondary infections? By secondary infection, I mean a challenge from a pathogen that is different from the one for which the vaccine was received.

For example, a person receives a dose of one of the SARS-CoV-2 mRNA vaccines, then, sometime during the critical period when circulating lymphocytes localize to the site of vaccination, the same person comes into contact with an influenza strain for which they have no adaptive immunity. Would that person have a lower chance of contracting flu had they not received the SARS-CoV-2 vaccine, all other factors being equal?

I found one publication that shows reduced risk for infection by influenza in patients who already had SARS-CoV-2, though this is attributed to pathogenic competition.4 Considering total pathogen dosage, it is logical to me that challenge with two pathogens is more likely to lead to illness than challenge with a single pathogen, but is there anything in the literature that suggests co-infection by an immunogenic "mock" pathogen (vaccine) and a secondary pathogen leads to a greater incidence of infection by the secondary pathogen?


References

  1. Mulligan, M.J., Lyke, K.E., Kitchin, N. et al. Phase I/II study of COVID-19 RNA vaccine BNT162b1 in adults. Nature 586, 589–593 (2020).
  2. Sahin, U., Muik, A., Derhovanessian, E. et al. COVID-19 vaccine BNT162b1 elicits human antibody and TH1 T cell responses. Nature 586, 594–599 (2020).
  3. Derek Thompson. The Pandemic’s Wrongest Man. The Atlantic, 1 April 2021.
  4. Stowe, J., Tessier, E., Zhao, H. et al. Interactions between SARS-CoV-2 and Influenza and the impact of coinfection on disease severity: A test negative design. medRxiv 2020.09.18.20189647.
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    $\begingroup$ Not an answer because I'm no immunologist at all (virologist though...) but the lymphocytes don't localize to the vaccination site, rather to secondary lymphocytic tissues - see here. The lymphopenia is a common occurrence in infection and vaccination and does not affect the antigen presenting cells already present from previous infections, only the pre-differentiation cells $\endgroup$
    – bob1
    Commented Apr 20, 2021 at 20:54
  • $\begingroup$ Thanks for your insight, bob1! I'll correct my question. If you're willing to expand on this in an answer, there's a bounty up for grabs. $\endgroup$
    – acvill
    Commented Apr 20, 2021 at 21:57
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    $\begingroup$ Unfortunately that's about as far as my knowledge of immunological processes goes. However, I think you will find that the answer is likely no - we are constantly under challenge from pathogens - think of all the bugs in your gut (E. coli) and on skin (Staph infections), inside your throat (strep) etc., and we don't see a sudden rise in these infections with vaccine programs. Note that anti-viral responses (CD8 T-cell) are slightly different to bacterial (CD4), though I don't know at which stage these play a role, though I suspect after the antigen-presenting stage. $\endgroup$
    – bob1
    Commented Apr 21, 2021 at 8:32
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    $\begingroup$ @bob1 - I would imagine that a significant challenge (what I imagine the OP is alluding to) would pertain only to response to another viral illness, not a bacterial infection, though the NYT reporter may not be implying that. $\endgroup$ Commented Apr 24, 2021 at 2:32
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    $\begingroup$ @acvill - Your question is a tiny bit misleading; yes, the number of lymphocytes circulating in peripheral blood decreases, we know that. The question should be (imo), "Does a lower peripheral lymphocyte count resulting from recent immunization render us more susceptible to infection by other viruses?" I can't answer that authoritatively, but decades of clinical experience leads me to lean towards "no". Interferons may be part of the reason. (I'm neither immunologist nor virologist, just a lowly FP/EM.) +1 for a well presented question. $\endgroup$ Commented Apr 24, 2021 at 2:42

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Mechanisms exist that could explain a higher susceptibility to virus B after or during a an infection of virus A, e.g. via targeted inhibition of anti-viral cellular mechanisms. In general, however, these anti-viral mechanisms favor an anti-correlation between infections of different viruses; e.g. up-regulation of interferons drastically reduces the probability of viruses to successfully complete their replication cycles. I once discussed with a leading virologist the possibility to use interferons as a general preventative treatment to temporarily prevent the spread of viral pandemics; I was told that this would theoretically work, but cannot be done due to enormous side-effects associated with them, i.e. ill feeling and depressions.

Similarly, activation of immune cells and the complement system by interleukins and C-reactive protein (CRP), that you mentioned, generally promote resistance against subsequent infections. CRP also promotes chemotaxis to the site of infection, which is why I would, similar to your source, understand chemotaxis as a sign of a good immune response. Examples like this are listed in the paper:

Mold et al. (69) showed that CRP provides mice with protection against infection by the gram-positive pathogen Streptococcus pneumoniae by binding to a PCh determinant of the pathogen cell wall and activating the complement pathway.

The complement system is also known to be effective in killing cells that are infected by viruses. Unfortunately, I could not find dedicated publication that connect lymphocyte migration with viral susceptibility, but my intuition is that lymphocyte migration should not be problematic when it comes to detecting viruses although it might contribute to the fact, that chronically elevated CRP levels are associated with the risk of cancer.

Importantly, one should not ignore behavioral aspects related to illness and vaccinations: There were reports of statistics, that people had significantly lower chances of being infected with CoV in the weeks between scheduling and receiving their first CoV shot, which was explained by individuals avoidance of risk. Reversely, people might loose their inhibitions concerning social distancing once they feel protected by vaccines, which could show up as a pseudo-susceptibility in statistics.

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