As the cell employs its machinery to shut down the virus that’s inside it, the virus makes proteins to shut down the cell’s efforts. The scene is set, but how will this arms race end? The answer depends on many, many factors.
Listeners can tune in to explore the following:
Since 2004, Matthew Frieman, PhD has been researching coronaviruses. In 2009, he established his own research lab at the University of Maryland School of Medicine, where he is an associate professor in the area of microbiology and immunology. First it was SARS-CoV, then MERS-CoV, and now SARS-CoV-2, the virus causing COVID-19. With each new coronavirus, he learns a little bit more about the tricks they use to enter and infect cells. He also learns more and more about therapeutics which could potentially combat the current virus and viruses to come.
A focal point of the research in Frieman’s lab is on the role of comorbidity in disease progression, and how an understanding of this in lab mice might be reflected in humans. For instance, why do those with underlying conditions appear significantly more vulnerable to SARS-CoV-2, and more likely to suffer severe symptoms? His research is also focused on developing a broadly antiviral drug not only for SARS-CoV-2, but for viruses that emerge in the future.
The conversation covers the similarities and differences between SARS-CoV-1 and SARS-CoV-2, two primary entry methods of SARS-CoV-2, the role of the ACE2 receptor and TMPRSS2 protease, why more virions per cell means fewer ACE2 receptors, which means decreased capacity for lung tissue repair, how cells detect the presence of a virus and respond accordingly, characteristics of viral spread, structure, and function, virus-host interactions, research aimed at combining antibodies to create a dual antiviral effect against SARS-CoV-2, and so much more.
Visit https://www.medschool.umaryland.edu/profiles/Frieman-Matthew/ and follow Frieman on Twitter @MattFrieman.
Available on Apple Podcasts: apple.co/2Os0myK