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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-thrombothic state associated to 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 COVID19 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.
Microvascular Inflammation
