The enigma of memory T cells in viral infections (including SARS-CoV-2)

Abstract

Viral infections and vaccinations produce immune responses mostly through B cells (plasmocytes/ antibodies) and effector T cells (helper and cytotoxic). After removing the antigen, 90-95% of the effector cells disappear, but the remaining ones turn into T cells with long memory. The maintenance of cellular memory, the mode of information storage and the lifespan of T cells are insufficiently known. After measles, resident T cells in the plasma will offer protection only against the measles virus, generating a long period of immunodepression (immune amnesia).After the flu, memory T cells generate immune protection for 1-2 years for secretory IgA and longer for serum IgG. In SARS-CoV-2 infection, memory T cells (B and T) respond quickly to reinfection for 8-10 months. In conditions of intense stimulation in SARS-CoV-2, SARS-CoV, MARS infection, marked leukopenia occurs with lymphopenia generating immunodepression and high mortality, disorders similar to septic shock. An important role in these disorders is played by the host's genetic structure and epigenome.