Viruses can induce autoimmune diseases, in addition to genetic predisposition and environmental
factors. Particularly, coronaviruses are mentioned among the viruses implicated in autoimmunity.
Today, the world's greatest threat derives from the pandemic of a new human coronavirus,
called “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2), the responsible
agent of coronavirus disease 2019 (COVID-19). COVID-19 originated in Wuhan, the capital of
Hubei, China, in December 2019 and, to date, has spread to at least 187 countries. This review focuses
on autoimmune manifestations described during COVID-19, including pro-thrombotic state
associated with antiphospholipid antibodies (aPL), acute interstitial pneumonia, macrophage activation
syndrome, lymphocytopenia, systemic vasculitis, and autoimmune skin lesions. This offers the
opportunity to highlight the pathogenetic mechanisms common to COVID-19 and several autoimmune
diseases in order to identify new therapeutic targets. In a supposed preliminary pathogenetic
model, SARS-CoV-2 plays a direct role in triggering widespread microthrombosis and microvascular
inflammation, because it is able to induce transient aPL, endothelial damage and complement activation
at the same time. Hence, endothelium might represent the common pathway in which autoimmunity
and infection converge. In addition, autoimmune phenomena in COVID-19 can be explained
by regulatory T cells impairment and cytokines cascade.