The article discusses whether severe covid19 cases arise from immunosuppression or a hyper-immune reaction, i.e. hyper-inflammation. Covid19 treatment may be different for patients with immunosuppression and patients with hyper-inflammation, because drugs that enhance the immune system may aggravate inflammation and drugs that suppress inflammation may suppress the immune system.
The immune system is less effective at fighting intracellular pathogens; thus, immune cells trigger excess inflammation and an inflammatory cascade. Chronic chlamydia infects immune cells, and in a series of innate immune responses, is able to infect T-cells. Immunosuppression in covid19 may occur when immune cells are previously infected with an intracellular pathogen, and/or the immune cells are co-infected with an intracellular pathogen and covid19. Infected immune cells are weaker, and produce less antibodies, which impairs the immune response. Covid19 may trigger hyper-inflammation when the immune cells are more prevalent and able to signal for a higher level of inflammation to fight covid19; or may re-ignite immune cells to signal for higher levels of inflammation to fight against the underlying intracellular pathogen and covid19.
Testing covid19 patients for chronic co-infections could reveal why some patients develop severe disease, some have immunosuppression, some have severe inflammatory reactions, and some have both. It could also lead to new alternatives for treatment, based on underlying chronic infections in covid19, which could explain immunosuppression, hyperinflammation, or both.
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