SARS-CoV-2 cell tropism and multiorgan infection

Abstract

Dear Editor,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.To elucidate SARS-CoV-2 tissue tropism, we used immunohistochemical and immunofluorescence staining.Results showed that viral antigens (spike proteins) were highly expressed in pneumocytes and hyperplastic cells around the bronchioles (Supplementary Fig. S1a-c); mucosal epithelia, submucosal glands, and gland ducts of the trachea (Supplementary Fig. S1d-f); mucosal epithelia and glands of the small intestine (Supplementary Fig. S1g,i); distal tubules and collecting ducts of the kidneys (Supplementary Fig. S1j-l); islets of Langerhans, glands, and intraislet ducts of the pancreas (Supplementary Fig. S1m,n); and