“Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a broad range of clinical responses including prominent microvascular damage. The capacity of SARS-CoV-2 to infect vascular cells is still debated. Additionally, the SARS-CoV-2 Spike (S) protein may act as a ligand to induce non-infective cellular stress. We tested this hypothesis in pericytes (PCs), which are reportedly reduced in the heart of patients with severe coronavirus disease-2019 (COVID-19). Here we newly show that the in vitro exposure of primary human cardiac PCs to the SARS-CoV-2 wildtype strain or the α and δ variants caused rare infection events...
... In conclusion, our findings suggest that the S protein may prompt PC dysfunction, potentially contributing to microvascular injury. This mechanism may have clinical and therapeutic implications.
Discussion: Our study provides novel proof-of-concept evidence for S protein to cause molecular and functional changes in human vascular PCs…
Conclusions: Although more in vivo investigation is needed, this work suggests that the S protein may elicit vascular cell dysfunction through CD147, independently from the infection. Blocking the CD147 receptor may help protect the vasculature of the most vulnerable patients from infection and the collateral damage caused by the S protein."
© Copyright 2023 Portland Press. This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). A commentary has been published: SARS-CoV-2 spike protein causes cardiovascular disease independent of viral infection