Thread by @Marc_Veld

Some #Immunology101:

A virus infection induces a strong T cell response. In the case of a virus; a type-1 response: involving Th1 cells and CD8 T cells. These cells are known to make the cytokine interferon-gamma (IFNg). They express activation markers, including PD-1.

When there is a heavy infection, there is a feedback mechanism. The T cells can now express interleukin-10 (IL-10). IL-10 is an inhibitory cytokine, which will dampen the response to try and limit immune-induced pathology/damage.

journals.aai.org/jimmunol/artic…

This is observed in many type-1 infections, as for SARS here above, and for the Malaria-causing parasite plasmodium here; where the IL-10 can also cause loss of the control of the lung microbiota. This loss of control can cause secondary infections.
nature.com/articles/s4146…

These secondary infections are well-known for influenza infections, where many do not die of influenza virus only, but of secondary bacterial or fungal infections.

journals.aai.org/jimmunol/artic…

As is also described here: but some will be fooled by reading the title only. What the paper shows in mice is a heavy H5N1 infection; very strong T cell activation, PD-1 is expressed, and yes, the cells express IL-10: they are highly stimulated.

journals.asm.org/doi/10.1128/JV…

This does not mean the response to influenza itself is per se suppressed: it is a attempt to spare further lung damage and is totally normal. It does come at a cost of slower viral clearance: but that is offset against not damaging your lungs too much! A excellent deal.

Indeed, subsequent infection with a slightly different influenza virus, that shares antigens, shows that the response is robust and protect the mice very well against reinfection.

The reason is that although the response is purposely curtailed to reduce damage, and as a consequence the virus is cleared later, and you make fewer memory T cells. But; you do make good amounts of memory T cells that rapidly expand when needed, and are very good at killing.

So; the immune response is purposely blunted; it means slower viral clearance, less memory T cells, but less lung damage! Subsequent challenge with a very similar virus for which memory T cells are protective, shows also no subsequent negative impact;

And this is what I mean. Scaremongering due to insufficient knowledge and not understanding the basic principles and context. Please be careful out there, don´t get fooled.