To boost or not to boost after infection ?

The answer is no.

I hope the reader is enjoying a very nice Saturday, and wish you a great Sunday. At this point, I am basically unofficially writing a series of B-cells and the vaccines, below are the previous 2 pieces.

Pre-existing immunity modulates responses to mRNA boosters

Failing Memory B cells from mRNA

Recent SARS-CoV-2 infection abrogates antibody and B-cell responses to booster vaccination

Per recent work of many other teams, authors go on to attempt to elucidate what is happening in the B cells (antibodies) department, since we are in uncharted territory with so many vaccination campaigns within a short period adding to the waves of reinfections within a short time.

Raising the point many did since 2020, wondering if repeated antigen stimulation by the exact same antigen would lead to the same deleterious effects as in other models, they wanted to find how this was actually faring. In line with the papers I shared, the immune response towards the vaccination besides being modulated by many other factors (including your glycemic state) is also modulated by prion infection.

Also for clarity's sake, these are all vaccinated, so we have prior-infected (prior to the vaccine), post-infected (vaccine after infection), and uninfected (vaccinated but never infected).

Prior SARS-CoV-2 infection restricts post-boost binding and neutralizing antibodies

These differences translated into higher fold increases between baseline and day 60 in the post-infected group compared to the two other groups and higher in the uninfected than prior-infected group), consistent with the antibody binding data. Overall, the kinetics and magnitude of antibody binding and neutralizing titers differed between the groups, although most strikingly in the prior-infected group where antibody responses to the booster vaccine were muted.

Prior SARS-CoV-2 infection restricts post-boost SARS-CoV-2 B-cell responses

Frequencies of B.1 RBD, NTD, as well as dual B.1/BA.1 RBD and NTD-binding B cells increased significantly from baseline to day 60 in the uninfected and post-infected groups, peaking at day 30 in the uninfected group while continuing to increase (RBD) in the postinfected group. In contrast, frequencies of spike-binding B cells in the prior-infected group did not significantly increase between baseline and day 30 and declined between days 30 and 60 against B.1 RBD and NTD and B.1/BA.1 NTD

As with antibody titers, baseline frequencies of spike-binding B cells were higher in the prior-infected than uninfected and post-infected groups for B.1 RBD and NTD and B.1/BA.1 RBD. At day 60, spike-binding frequencies were similar between the prior-infected and uninfected group yet were lower for B.1 RBD and B.1/BA.1 RBD in both groups when

We then considered whether post-boost BA.1 infection and/or the booster vaccine altered the ratio of dual B.1/BA.1 to single B.1 RBD or NTD binding. For RBD, the ratio of dual B.1/BA.1 to single B.1 binding increased from baseline to day 60 in all three groups; however, the ratio was highest in the post-infected group and lowest in the prior-infected group . For NTD, the ratios increased from baseline to day 60 in the uninfected and post-infected but not prior-infected group and at day 60, and the ratios at day 60 were similarly higher in the uninfected and post-infected than in the prior-infected group. Overall, the B-cell response to the booster vaccine was poor in magnitude and breadth in the prior-infected group while robust in the uninfected and post-infected groups, with the latter having an additional boost from the breakthrough infection.

So this doesn’t become overly complex, and hard to follow for the average Joe (and also unnecessarily gigantic), I will cover the main point, but will leave this portion of the data here.

They measure different markers at different time intervals, which you can see in the graph 0, 30, 60 (days), and they found that people priorly infected, had antibody response differences in both binding and neutralizing, with the most starking one being among the prior-infected group, where the booster (vaccine after infection) was “muted” meaning a poorer response, quicker waning.

A similar trend was found in post-booster B cell responses, where once again, prior infected people had a poorer response in both breadth (number of important targets to which antibodies were made) and magnitude (antibody level measured, quantity) in the prior-infected group leading credence to the paper stating prior infection antibodies can out compete vaccine ones. Also, an interesting point was that prior infected people had the B cell response measure here wane quicker than the other groups, another point raised where you shouldn’t take the vaccine if you were ever infected between 2020 and 2021.

Prior SARS-CoV-2 infection restricts post-boost memory B-cell derived antibodies

To gain further insight into B-cell VOC responses after booster vaccination and the effect of post-boost BA.1 infection, we performed in vitro culturing of peripheral blood mononuclear cells (PBMCs) at baseline and day 60 using polyclonal stimuli known to favor memory B-cell differentiation and antibody secretion.

Overall, spike-specific antibodies secreted from memory B cells did not increase in the prior-infected group after the vaccine boost and while levels compared to both uninfected and post-infected groups were similar or modestly higher at baseline, they were sharply lower by day 60.

Collectively, these findings suggest that prior to booster vaccination, spike-specific B cells of recently infected individuals are more poised to respond to stimulation than those of uninfected individuals yet are refractory to further stimulation following vaccination.

I can’t be bothered to go digging into dozens of papers, but contrary to the non-science pushed by many of the vaccine enthusiasts, boosting after an infection has literally no benefit and in fact, hinders the response from people who were priorly infected.

The researchers go to further test the changes in B Cell responses and phenotypes, they test this by using specific markers (tyrosine kinase Syk and phospholipase Cg2), leading them to find distinct responses between the 3 different groups.

The entire paper has a severe, and clear bias towards the obvious (vaccine is good, safe, and effective), but it gives a lot of information and good data to go through. In line with other papers, but measuring using different methodology authors found that a similar result as the other papers covered recently, that your infection status will play a larger and dominant role over how your body will respond to the vaccines.

There is increasing evidence that I was meant to cover but didn’t, that the vaccines do cause a shift in response in many levels of the immune system, with a clear division between the vaccinated and not vaccinated, and I am not arguing here about effectiveness, merely the cellular and mechanistic response. It is undeniable that infection with any Omicron variant is a good defense against further infection and severity from future Omicrons, so why would you lock someone into a smaller epitope range by vaccinating after said infection (the last paragraph highlighted in the second image).

The closing remarks by the authors make the case itself. And as a reminder, it has been known forever, and for over 18 months that you need T Cell immunity to properly deal with SARS-CoV-2, especially to clean the virus from your body.

With the increasing amount of evidence, there is no reason to boost or take a vaccine after an Omicron infection, especially with early treatment, and continuously boosting will have a long-term, broader effect on overall immunity (immunological shift).

Massive appreciation to all supporters here and on Kofi !!!