This study by researchers at Brown University, Providence, Rhode Island, reveals the cellular mechanism behind why the elderly and patients with preexisting conditions are at higher risk of infection, severe side effects, and death from COVID-19.
The researchers detail their discovery that circulating levels of a protein called chitinase 3-like-1 (CHI3L1) increase with age, comorbid diseases, and infection, and that CHI3L1 is a potent stimulator of the receptor ACE2, the spike protein that SARS-CoV-2 uses to enter human cells.
The researchers also developed a monoclonal antibody (FRG) that attaches to a particular region of CHI3L1. They found that this antibody and another small molecule blocked the induction of the ACE2 receptor.
The findings support the concept that CHI3L1 plays a critical role in the pathogenesis of COVID-19, and they provide an explanation of how aging and comorbid diseases contribute to the pathogenesis of COVID-19, the authors say. The findings also have implications for the development of therapeutics to control COVID-19 infection.Read More >>