Endothelial cells are not productively infected by SARS-CoV-2.

ABSTRACT:

Objectives

Thrombotic and microvascular complications are frequently seen in deceased COVID-19 patients. However, whether this is caused by direct viral infection of the endothelium or inflammation-induced endothelial activation remains highly contentious.

Methods

Here, we use patient autopsy samples, primary human endothelial cells and an in vitro model of the pulmonary epithelial-endothelial cell barrier.

Results

We show that primary human endothelial cells express very low levels of the SARS-CoV-2 receptor ACE2 and the protease TMPRSS2, which blocks their capacity for productive viral infection, and limits their capacity to produce infectious virus. Accordingly, endothelial cells can only be infected when they overexpress ACE2, or are exposed to very high co

SUBMITTER: Schimmel L 

PROVIDER: S-EPMC8542944 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature