SARS-CoV-2 Spike protein binds to heart’s vascular cells potentially contributing to severe microvascular damage

Press release issued: 3 February 2022

A new study has shown how SARS-CoV-2 may contribute to severe microvascular damage seen in severely-ill COVID-19 patients by transforming human heart vascular cells into inflammatory cells, without infecting them. The University of Bristol-led research, published in Clinical Science, indicates blocking antibodies could represent a new treatment to alleviate cardiovascular complications.

In this new study, a multidisciplinary research team from the University’s Bristol Heart Institute sought to investigate how SARS-CoV-2 interacts with heart cells causing the myocardial damage seen in COVID-19 patients. Until now, it remained unclear whether heart cells are infected by the virus or damaged because of an excess cytotoxic defence response. This response, also known as ‘the cytokine storm’, comes from our immune cells, whereby cytotoxic cells attack and kill the infected cells by releasing proteins, called cytokines. The team also sought to investigate whether heart cells contribute to producing excess cytokines.

Read the full University of Bristol press release

Paper: ‘The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease’ by Elisa Avolio et al in Clinical Science.