Seminar: Stefan Pöhlmann

The 3As of SARS-CoV-2 infection: ACE2, antibodies and activators

I am interested in virus–host cell interactions, particularly in how emerging viruses enter their target cells. My laboratory has shown that enveloped viruses exploit cellular lectins for attachment and infection and may use lectin-expressing cells to facilitate dissemination. We identified ACE2 as the receptor for human coronavirus NL63 and discovered that the serine protease TMPRSS2 activates coronaviruses for host cell entry. During the COVID-19 pandemic, we demonstrated that ACE2 and TMPRSS2 are essential for SARS-CoV-2 infection of lung cells and that their use explains the failure of hydroxychloroquine as a COVID-19 drug. We also identified a unique furin cleavage site in the SARS-CoV-2 spike protein and showed that it is critical for lung cell infection. Our work further revealed that SARS-CoV-2 variants evolve under antibody pressure, that Omicron evades antibodies with exceptional efficiency, and that new variants can reacquire virulence factors present in early pandemic strains.