| First Author | Lambertz RLO | Year | 2020 |
| Journal | Virol J | Volume | 17 |
| Issue | 1 | Pages | 56 |
| PubMed ID | 32321537 | Mgi Jnum | J:302402 |
| Mgi Id | MGI:6508251 | Doi | 10.1186/s12985-020-01323-z |
| Citation | Lambertz RLO, et al. (2020) H2 influenza A virus is not pathogenic in Tmprss2 knock-out mice. Virol J 17(1):56 |
| abstractText | The host cell protease TMPRSS2 cleaves the influenza A virus (IAV) hemagglutinin (HA). Several reports have described resistance of Tmprss2(-/-) knock-out (KO) mice to IAV infection but IAV of the H2 subtype have not been examined yet. Here, we demonstrate that TMPRSS2 is able to cleave H2-HA in cell culture and that Tmprss2(-/-) mice are resistant to infection with a re-assorted PR8_HA(H2) virus. Infection of KO mice did not cause major body weight loss or death. Furthermore, no significant increase in lung weights and no virus replication were observed in Tmprss2(-/-) mice. Finally, only minor tissue damage and infiltration of immune cells were detected and no virus-positive cells were found in histological sections of Tmprss2(-/-) mice. In summary, our studies indicate that TMPRSS2 is required for H2 IAV spread and pathogenesis in mice. These findings extend previous results pointing towards a central role of TMPRSS2 in IAV infection and validate host proteases as a potential target for antiviral therapy. |
