tetano
Editor, Senior Moderator
J Gen Virol. 2019 May 17. doi: 10.1099/jgv.0.001274. [Epub ahead of print]
[h=1]Tmprss2 knock-out mice are resistant to H10 influenza A virus pathogenesis.[/h] Lambertz RLO[SUP]1[/SUP], Gerhauser I[SUP]2[/SUP], Nehlmeier I[SUP]3[/SUP], Leist SR[SUP]1[/SUP], Kollmus H[SUP]1[/SUP], P?hlmann S[SUP]4,[/SUP][SUP]3[/SUP], Schughart K[SUP]5,[/SUP][SUP]6,[/SUP][SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]-/-[/SUP] 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[SUP]-/-[/SUP] mice were reduced compared to wild-type mice. In addition, no viral antigen was detected in the lungs of Tmprss2[SUP]-/-[/SUP] 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.
PMID: 31099738 DOI: 10.1099/jgv.0.001274
[h=1]Tmprss2 knock-out mice are resistant to H10 influenza A virus pathogenesis.[/h] Lambertz RLO[SUP]1[/SUP], Gerhauser I[SUP]2[/SUP], Nehlmeier I[SUP]3[/SUP], Leist SR[SUP]1[/SUP], Kollmus H[SUP]1[/SUP], P?hlmann S[SUP]4,[/SUP][SUP]3[/SUP], Schughart K[SUP]5,[/SUP][SUP]6,[/SUP][SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]-/-[/SUP] 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[SUP]-/-[/SUP] mice were reduced compared to wild-type mice. In addition, no viral antigen was detected in the lungs of Tmprss2[SUP]-/-[/SUP] 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.
PMID: 31099738 DOI: 10.1099/jgv.0.001274