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J Gen Virol. 2019 Jul;100(7):1073-1078. doi: 10.1099/jgv.0.001274. Epub 2019 May 17.

Tmprss2 knock-out mice are resistant to H10 influenza A virus pathogenesis.

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1 Department of Infection Genetics, Helmholtz Centre for Infection Research, Braunschweig, Germany.
2 Department of Pathology, University of Veterinary Medicine Hannover, Hannover, Germany.
3 Infection Biology Unit, German Primate Center - Leibniz Institute for Primate Research, Göttingen, Germany.
4 Faculty of Biology and Psychology, University Göttingen, Göttingen, Germany.
5 University of Veterinary Medicine Hannover, Hannover, Germany.
6 Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee, USA.


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.


H10; Influenza A virus; TMPRSS2; host protease


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