TABLE 3.

Pre‐existing factors conditioning innate and adaptive responses to SARS‐CoV‐2 infection

Genetic (or epigenetic) polymorphisms of TLR, TLR signaling, type I/III IFN, and IFNR and their signaling, ‘C factors, Inflammasome components

HLA‐E haplotypes and expression of KLRC gene (encoding NKG2C) conditioning trained memory NK cells

HLA haplotypes binding the viral superantigens

HLA haplotypes presenting viral epitopes, including that cross‐reacting with self‐antigens

Degree of pre‐existing immunity to cross‐reacting epitopes of common cold coronaviruses

Naïve T/memory T cells ratio (children vs elderly people)

Proportion of Innate memory IgM+B cells producing natural Abs cross reacting with SARS‐CoV‐2

Susceptibility genes for autoimmunity conditioning the derangement of peripheral tolerance, the proportion of autoreactive bystander T and B cells, Treg cell function and ease to produce pathogenic autoantibodies

Bone‐marrow reservoir of inflammatory precursors (mobilized by inflammatory molecules) able to develop rapid NK and T cell progenies

Bone marrow reservoir of neutrophil precursors with immunosuppressive function

Not stabilized co‐morbidities displaying uncontrolled inflammation

Abbreviations: Abs, antibodies; IFN, interferon; IFNR, interferon receptor; NK, natural killer; TLRs, Toll‐like receptors; Treg, T regulatory.