2. Autoimmune diseases / syndromes potentially associated with Covid-19 described so far It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or

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. Cell death and the subsequent post-mortem changes, called necrosis, are integral parts of normal development and maturation cycle. Despite the importance of this process, the mechanisms underlying cell death are still poorly understood. In the recent literature, cell death is said to occur by two alternative, opposite modes: apoptosis, a programmed, managed form of cell death, and necrosis, an unordered and accidental form of cellular dying. The incorrect consequence is the overlapping of: a) the process whereby cells die, cell death; and b) the changes that the cells and tissues undergo after the cells die. Only the latter process can be referred to as necrosis and represents a 'no return' process in cell life. In this review, we discuss the excellent basic research developed in this field during last decades and problems that remain to be resolved in defining both experimentally and mechanicistically the events that lead to and characterize cell death. IntroductionCell death is part of normal development and maturation cycle, and is the component of many response patterns of living tissues to xenobiotic agents (i.e. micro organisms and chemicals) and to endogenous modulations, such as inflammation and disturbed blood supply (1,2). Cell death is an important variable in cancer development, cancer prevention and cancer therapy (3-5). In the treatment of cancer, the major approach is the removal, by surgery, of the neoplasm and/or the induction of cell death in neoplastic cells by radiation, toxic chemicals, antibodies and/or cells of the immune system (6-9). On the other hand, this pathobiological process remains poorly understood and the physiological and biochemical factors that lead to cell death are still not clear. One main factor is the existing confusion between 'apoptosis' process, as compared and contrasted with 'necrosis', leading to the overlapping of the ante mortem changes, i.e. the process of cell death, and the post-mortem changes, i.e. the necrosis process. The pathobiology of cell deathThe elegant scientific exploration of sub-cellular molecular anatomy of the last decades have reinforced the cell concept as 'the smallest integrating unit in biology: a pseudo-intelligent computer that receives, screens, changes, reacts to and adapts to a host of environmental signals, all of this activity apparently

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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection is linked to a respiratory syndrome with altered pulmonary and alveolar function that can lead to acute respiratory insufficiency and even death [1]. The molecular determinants and the mechanism that link SARS coronavirus infection to the pulmonary pathology are unknown. The scientific-clinical picture is further complicated by the fact that, while human SARS CoVs presents heavy pathogenicity leading to death [1], other human CoVs, such as HCoV-OC43 and HCoV-229E, are less pathogenic and cause common colds and mild lower respiratory tract infections [2].Here, we explore the issue based on the rationale that, following a pathogen infection, peptide commonalities between the pathogen and the human proteins might trigger cross-reactions and a pathologic autoimmune sequela that might contribute to explain the pathogen associated diseases [3]. Accordingly, we started the present study by investigating the spike glycoproteins from both SARS-CoV-2 and HCoV-229E for peptide sharing with human surfactant and related proteins. J o u r n a l P r e -p r o o f Journal Pre-proof