| First Author | Beck S | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 450 | PubMed ID | 32231671 |
| Mgi Jnum | J:306211 | Mgi Id | MGI:6706142 |
| Doi | 10.3389/fimmu.2020.00450 | Citation | Beck S, et al. (2020) ANP32B Deficiency Protects Mice From Lethal Influenza A Virus Challenge by Dampening the Host Immune Response. Front Immunol 11:450 |
| abstractText | Deciphering complex virus-host interactions is crucial for pandemic preparedness. In this study, we assessed the impact of recently postulated cellular factors ANP32A and ANP32B of influenza A virus (IAV) species specificity on viral pathogenesis in a genetically modified mouse model. Infection of ANP32A(-/-) and ANP32A(+/+) mice with a seasonal H3N2 IAV or a highly pathogenic H5N1 human isolate did not result in any significant differences in virus tropism, innate immune response or disease outcome. However, infection of ANP32B(-/-) mice with H3N2 or H5N1 IAV revealed significantly reduced virus loads, inflammatory cytokine response and reduced pathogenicity compared to ANP32B(+/+) mice. Genome-wide transcriptome analyses in ANP32B(+/+) and ANP32B(-/-) mice further uncovered novel immune-regulatory pathways that correlate with reduced pathogenicity in the absence of ANP32B. These data show that ANP32B but not ANP32A promotes IAV pathogenesis in mice. Moreover, ANP32B might possess a yet unknown immune-modulatory function during IAV infection. Targeting ANP32B or its regulated pathways might therefore pose a new strategy to combat severe influenza. |
