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Repeated doses of mRNA vaccine bias the antibody response to a less inflammatory IgG4 subtype. These antibodies still neutralise the virus, but some other effector functions are reduced.
What could this mean for future #COVID19 vaccine policy? Helpful commentary here by the legendary Shiv Pallai: is it bad, is it good, or is #IgG4 just misunderstood?
@travelhealthdoc thanks for the link.
Thanks for sharing this! I have wondered about this, but hadn't seen it discussed much. Whenever that happens I just assume that not having a bio background has left me without some key knowledge and I wait for the more well versed amongst us to discuss it so I can learn.
Perhaps @fitterhappierAJ could weigh in?
@BE @fitterhappierAJ I'm not sure if it's a cause for concern: it's just quite interesting immunologically.
All the clinical evidence shows that currently-available mRNA boosters are effective in preventing death and hospitalisation.
The suggestions in the article on ways to tweak boosters in the future look sensible.
To be clear, I didn't express concern, per se. I know there's this rush to defend vaccinations anytime anything even slightly negative is brought up, and so I don't generally mention the v-word at all. I do all of my COVID advocacy on that tightrope.
I'm honestly interested in the timing, and exactly this science, when multiple things are seemingly fairly clear:
We can't vaxx our way out of this alone.
The vaccines do work for lowering(not preventing...lets not start the whole vaxx and relax thing again) death and hospitalization.
Antibodies seem to wane far sooner than a year.
The administration wants to do yearly vaccines.
Science like this article discusses seems to indicate that vaccinating every few months, when antibodies wane, might not be the best idea.
There's seemingly a conundrum there that I'm not sure health policy has thought through just yet. I'm always open to new science and new trains of thought!
@BE That's fair - you did not 
I think collectively we are still figuring out how best to deal with this disease in the longer term
Oh absolutely. There's virtually no way to know everything we need to know at this point. Science just doesn't work that way.
I just want to see the discussion had at each step, rather than trying to skip steps along the way. If that makes sense.
1)The Nucleocapsid is highly pernicious. Dysregulated Antibody Dependent Complement Mediated Lysis of the SARS-CoV-2 virion is the cause of Severe Disease for the overwhelming majority of those afflicted.
IgG4 discourages ADCML relative to other subtypes because it has the lowest affinity for C1q. This encourages Antibody Dependent Cellular Phagocytosis by default.
However, this is an indirect effect as Spike ABs don't necessarily effect lysis of the
2)lipid portion of the viral envelope. That falls to M-protein ABs. Still, decreased demand on C1-INH by that IgG4 is going to make more C1-INH available in the microenvironment to slow down M-protein dependent ADCML, so it is still a win.
What would be really nice is IgG4 on the M-protein epitopes. Or better yet, aptamers without FCs altogether.
I'm still a little slow with all of the immunology ins and outs but I got there. Thank you for the thoughts, as always!