SARS-CoV-2 cell tropism and multiorgan infection

Abstract

To date, the number of confirmed coronavirus disease 2019 (COVID-19) cases has surpassed 100 million, with deaths exceeding 2 million, yet the mechanism by which severe acute respiratory syndrome coronavirus (SARS-CoV)-2 attacks the body remains unclear. Although SARS-CoV-2 is known to primarily target the lung, it is also believed to cause multi-organ dysfunction and comprehensive studies on SARS-CoV-2 cell tropism in humans are lacking. SARS-CoV-2 exploits the host angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entry 1 , but the correlation between SARS-CoV-2 organ/cell tropism and ACE2 distribution is unclear. Here, we studied these issues via a systemic analysis of postmortem specimens from a 66-year-old female COVID-19 patient who had rapidly developed multiorgan failure. The patient died in the hospital on Day 13 of admission (Day 16 of illness) and her autopsy was performed at 8 h after death.

Cited by papers we hold 3

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• SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein · 2022
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• SARS-CoV-2 infection produces chronic pulmonary epithelial and immune cell dysfunction with fibrosis in mice · 2022
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