COVID-19: Respiratory Distress and the Overactive Immune Response
By Rowena Johnston, Ph.D.
amfAR’s Dr. Jeffrey Laurence publishes findings that could point the way to therapeutic interventions
Dr. Jeffrey Laurence is amfAR’s senior scientific consultant.One of the hallmark features of COVID-19 is shortness of breath that can become life-threatening. Until recently, it was thought that this respiratory distress was similar to classic acute respiratory distress syndrome, or ARDS, which can occur in pneumonia or after traumatic lung injury.
However, doctors noted that the respiratory distress seen in COVID-19 differs from classic ARDS in at least one important respect, namely that the lungs of COVID patients can still expand and contract the way healthy lungs do. The shortness of breath in COVID is due to the air sacs of the lungs becoming filled with fluid and dead cells. Therefore, the pathology in the lungs of COVID-19 patients was likely to differ substantially from that seen in other types of ARDS, including the original SARS epidemic.
amfAR’s senior scientific consultant for programs, Dr. Jeffrey Laurence, working with colleagues, was one of the first to describe this difference, and then to define the underlying immune mechanisms of the phenomenon. They discovered a strikingly high level of a complement—a set of proteins that facilitate clearance of infections—in small blood vessels.
More specifically, they identified a precise collection of complement and associated proteins that appear to play an important role in the overactive immune response that characterizes the severe manifestations of COVID-19. These findings point the way to potential therapeutic interventions to help prevent mortality in COVID-19.
The research was published in the April 15 issue of Translational Research and was featured in a news story in the prestigious journal Nature.
Dr. Johnston is vice president and director of research at amfAR.