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Abstract :

Coronavirus disease 2019 (COVID-19), caused by coronavirus severe acute respiratorysyndrome coronavirus 2 (SARS-CoV-2), has caused extensive disruption and mortality since its recent emergence. Concomitantly, there has been a race to understand thevirus and its pathophysiology. The clinical manifestations of COVID-19 are manifoldand not restricted to the respiratory tract. Extrapulmonary manifestations involvingthe gastrointestinal tract, hepatobiliary system, cardiovascular and renal systems havebeen widely reported. However, the pathophysiology of many of these manifestationsis controversial with questionable support for direct viral invasion and an abundanceof alternative explanations such as pre-existing medical conditions and critical illness.Prior research on SARS-Co-V and NL63 was rapidly leveraged to identifyangiotensin-converting enzyme 2 (ACE2) receptor as the key cell surface receptor forSARS-CoV-2. The distribution of ACE2 has been used as a starting point for estimating vulnerability of various tissue types to SARS-CoV-2 infection. Sophisticatedorganoid and animal models have been used to demonstrate such infectivity ofextrapulmonary tissues in vitro, but the clinical relevance of these findings remainsuncertain. Clinical autopsy studies are typically small and inevitably biased towardspatients with severe COVID-19 and prolonged hospitalization. Technical issues suchas delay between time of death and autopsy, use of inappropriate antibodies forparaffin-embedded tissue sections and misinterpretation of cellular structures as virusparticles on electron micrograph images are additional problems encountered in theextant literature. Given that SARS-CoV-2 is likely to circulate permanently in humanpopulations, there is no doubt that further work is required to clarify the pathobiologyof COVID-19