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Updated: Jan 24, 2026

Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Tmprss2 knock-out mice are resistant to H10 influenza A virus pathogenesis
Ruth L O Lambertz1, Ingo Gerhauser2, Inga Nehlmeier3
11 Department of Infection Genetics, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Abstract:
The surface protein haemagglutinin (HA) of influenza A viruses (IAV) needs to be cleaved by a host protease to become functional. Here, we investigated if IAV of the H10 subtype also requires TMPRSS2 for replication and pathogenesis in mice. We first showed in cell culture that TMPRSS2 is able to cleave H10-HA. When Tmprss2-/- deficient mice were infected with a re-assorted virus H10-HA, they did not lose body weight and no viral replication was observed in contrast to wild-type mice. Histopathological analysis showed that inflammatory lesions in the lung of Tmprss2-/- mice were reduced compared to wild-type mice. In addition, no viral antigen was detected in the lungs of Tmprss2-/- mice and no evidence for HA cleavage was observed. We conclude from these studies that TMPRSS2 activity is also essential for in vivo replication and pathogenesis of H10 IAV.
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