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MoreTrueStories t1_is85li9 wrote

Reply to comment by ZSpectre in SARS-CoV2 enters the brain through the olfactory nerve in rhesus monkeys, causing neuroinflammation. The virus spread further into the brain in aging animals. by andyhfell

Allergies are one of the leading causes of sinus infections (which are typically caused by viruses). That suggests that inflammation will not impede, but rather precipitate the infectivity of SARS-CoV-2.

Following infection, a systemic immune response is mounted, characterized by increased serum concentrations of chemokines and pro-inflammatory cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF), and the appearance of activated monocytes, followed by SARS-CoV-2-specific immunoglobulin M (IgM), IgA, and IgG antibodies and interferon-γ-producing T cells. This concerted action of the immune system controls the replication of SARS-CoV-2.

With that said, the question is whether or not the preexisting inflammation would also result in the immune system detecting the virus earlier than it would in subjects without active allergies. It does seem likely that patients with already elevated levels of immunoglobulin would help detect the virus sooner and would likely result in better outcomes (i.e. no PACs 'long covid).

/u/Anthrogal11 my hypothesis is that you would have a higher rate of infection but also be more likely to present as asymptomatic. Something that may confound the above is if your allergies are so bad that they significantly restrict airflow through your sinuses.

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ZSpectre t1_isauhp8 wrote

Thanks a ton for the reply. If I'm getting what you're saying correctly (and this may be a fun review of immunology for me since I was no big fan of the subject back in the day), I'm first thinking of an analogy comparing the difference between a walled fortress with a few soldiers versus one that would only have a small fence but a ton more soldiers, weapons, and tracking devices. For those passing by, the walled fortress would be like the blood vessel's "normal state" while the latter would be the "inflamed" state seen both in allergies and active infection.

While someone with allergies would have the latter state much more often with the weakened barrier (inflammation causes more porous blood vessels likely to function as a means to let more white blood vessels come in), I'm first guessing that this would be the main reason why it would precipitate the infectivity of viruses that happen to come by (as said in your first point).

In other words, all viruses that get into the upper nose may have an easier time getting through the small fence. And while the ones that cause allergic rhinitis may have an easier time evading the soldier's detection systems (perhaps more nimble / more stealthy), the question all 3 of us are talking about is whether or not SARS-CoV-2 may have a more difficult time avoiding getting tagged by the soldier's detection systems despite more easily getting in. (compared to a normal person who starts out with the walled fortress, maybe the virus may have a tougher time coming in, but if they ever do, the soldiers would have to go through "normal protocol" of calling for back up, weapons, and tagging systems, which all could take up extra time)

And to translate your hypothesis, perhaps much more SARS-CoV-2 viruses get in with a weak fence, but they likely won't do much after that since perhaps getting tagged more easily would make the rest the soldiers in the other fortresses much more aware of their presence (even if they get to other parts of the body, they have a shining beacon on them). The confounder is how allergies may just so happen to supplement the weak fenced compound with a big wall of slime.

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