Authors: Theoharides TC

PMID: 32339387 PMCID: PMC7267424 DOI: 10.1002/biof.1633

Abstract

The new coronavirus (severe acute pulmonary syndrome [SARS]‐CoV‐2) originated in China, where it spread rapidly, and has reached pandemic proportions because of its high rate of infectivity as well as high morbidity and mortality, associated with COVID‐19. This coronavirus infects by first binding to the ectoenzyme angiotensin‐converting enzyme 2 (ACE2), a serine protease acting as the receptor, while another serine protease is necessary for priming the viral “S” protein required for entering the cells. Defense against the virus apparently does not involve inflammatory cytokines, but pulmonary infection and its serious sequelae result from the release of multiple chemokines and cytokines that damage the lungs.

Keywords: SARS-CoV-2, COVID-19, pulmonary mast cells, cytokine storms, luteolin