Bioactive lipids in antiviral immunity

Abstract

Lipids may influence viral entry, replication, and clearance and modulate immune responses Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has brought focus to attempts to limit viral replication and manage the immunological response to infection. Lipids modulate host receptor binding, facilitate viral fusion, and fuel viral replication; thus, modulation of viral-host lipid interactions may have therapeutic utility (1). Indeed, the spike (S) glycoprotein on the surface of SARS-CoV-2 tightly binds the free fatty acid linoleic acid, stabilizing it and reducing its interaction with the host angiotensin-converting enzyme 2 (ACE2) receptor that facilitates viral cell entry (2). However, in the case of many viral infections, including COVID-19, it is the overexuberant host immune response that results in life-threatening consequences of infection. Therefore, therapies that modulate bioactive lipids that regulate the host immune response to respiratory viral infections may be beneficial.