Related paper in Lancet:
Lancet. 2020 395(10234): 1417–1418.
Endothelial cell infection and endotheliitis in COVID-19
Zsuzsanna Varga,a Andreas J Flammer,b Peter Steiger,c Martina Haberecker,a Rea Andermatt,c Annelies S Zinkernagel,d Mandeep R Mehra,e Reto A Schuepbach,c Frank Ruschitzka,b and Holger Mocha
Cardiovascular complications are rapidly emerging as a key threat in coronavirus disease 2019 (COVID-19) in addition to respiratory disease. The mechanisms underlying the disproportionate effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on patients with cardiovascular comorbidities, however, remain incompletely understood.
1,
2
SARS-CoV-2 infects the host using the angiotensin converting enzyme 2 (ACE2) receptor, which is expressed in several organs, including the lung, heart, kidney, and intestine. ACE2 receptors are also expressed by endothelial cells.
3 Whether vascular derangements in COVID-19 are due to endothelial cell involvement by the virus is currently unknown. Intriguingly, SARS-CoV-2 can directly infect engineered human blood vessel organoids in vitro.
4 Here we demonstrate endothelial cell involvement across vascular beds of different organs in a series of patients with COVID-19 (further case details are provided in the
appendix).
Patient 1 was a male renal transplant recipient, aged 71 years, with coronary artery disease and arterial hypertension. The patient’s condition deteriorated following COVID-19 diagnosis, and he required mechanical ventilation. Multisystem organ failure occurred, and the patient died on day 8.
Post-mortem analysis of the transplanted kidney by electron microscopy revealed viral inclusion structures in endothelial cells (
figure A, B ). In histological analyses, we found an accumulation of inflammatory cells associated with endothelium, as well as apoptotic bodies, in the heart, the small bowel (
figure C) and lung (
figure D). An accumulation of mononuclear cells was found in the lung, and most small lung vessels appeared congested.