The severe acute respiratory syndrome coronavirus−2 (SARS-CoV-2) has been recently identified as the culprit of the highly infectious, outbreak named coronavirus disease 2019 (COVID-19) in China. Now declared a public health emergency, this pandemic is present in more than 200 countries with over 14 million cases and 600,000 deaths as of July 18, 2020. Primarily transmitted through the respiratory tract, the most common clinical presentations of symptomatic individuals infected with SARS-CoV-2 include fever, dyspnea, cough, fatigue, and sore throat. In advanced cases, patients may rapidly develop respiratory failure with acute respiratory distress syndrome, and even progress to death. While it is known that COVID-19 manifests similarly to the 2003 Severe Acute Respiratory Syndrome (SARS) and the 2012 Middle East Respiratory Syndrome (MERS), primarily affecting the pulmonary system, the impact of the disease extends far beyond the respiratory system and affects other organs of the body. The literature regarding the extrapulmonary manifestations (cardiovascular, renal, hepatic, gastrointestinal, ocular, dermatologic, and neurological) of COVID-19 is scant. Herein, we provide a comprehensive review of the organ-specific clinical manifestations of COVID-19, to increase awareness about the various organs affected by SARS-CoV-2 and to provide a brief insight into the similarities and differences in the clinical manifestations of COVID-19 and the earlier SARS and MERS.

Using RNA hybridization techniques, we examined the expression of proto-oncogenes associated with lymphocyte activation in vitro in patients with systemic lupus erythematosus and other autoimmune diseases. T and B lymphocytes from these patients were found to have significantly increased expression of c-myc, c-myb, and c-ruf RNA when compared with those of normal individuals. Among the mononuclear cell subpopulations, B lymphocytes expressed higher levels of RNA for these proto-oncogenes compared with the T lymphocytes. Since prompt expression of these and other protooncogenes occurs in fibroblasts and lymphocytes following mitogenic stimulation, we propose that the present findings reflect the pathologically activated state of various lymphocytic subpopulations which is observed in systemic lupus erythematosus and in other autoimmune diseases. Endogenous and exogenous factors which lead to the expression of autoimmunity might share the induction of proto-oncogene expression as a common pathogenetic step.Human systemic autoimmune disorders are characterized by altered immunologic functions and the production of multiple autoantibodies. In the most

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