Fig. 1

The figure describes the structure of SARS-CoV2 and the possible infection associated mechanism of autoimmunity. SarsCov2 infects epitelial cells by receptors angiotensin converting enzyme 2 (ACE2) resulting in replication and release of the virus with consequent pyroptosis and the release of damage associated molecular patterns. This process leads to local inflammation and secretion by alveolar macrophages of pro-inflammatory cytokines such as IL-6, IL-10, macrophages inflammatory protein 1 alfa (MIPa), and TNF. Furthermore, this figure describes epitope spreading where persistent infection leads to the uptake of microbial antigens by antigen presenting cells (APCs) and antigen presentation of T-cells. This mechanism carries an inflammatory cascade resulting in a tissue damage, a possible uptake of self-antigens by APC and subsequent presentation of these self-antigens to Tc ells causing an anti-self-reaction. After microbial infection self-antigens could be recognised and processed by APC; subsequently cryptic epitopes could be exposed and presented to self-reactive T-cells leading to an autoimmune response. This figure also describes the mechanism of molecular mimicry where microbial antigens could share antigenic similarly with self-antigens. The presentation of these self-antigen mimics by APC to cross reactive cells leads to an inflammatory response because T cells recognize both the microbial mimic and its respective self-antigens. Finally, viral particles and proinflammatory cytokines induce the activation of blood monocytes which respond by inducing tissue factor membrane expression contributing to a pro-thrombotic state