Choonnasard, A.; Shofa, M.; Okabayashi, T.; Saito, A. Conserved Functions of Orthohepadnavirus X Proteins to Inhibit Type-I Interferon Signaling. Int. J. Mol. Sci.2024, 25, 3753.
Choonnasard, A.; Shofa, M.; Okabayashi, T.; Saito, A. Conserved Functions of Orthohepadnavirus X Proteins to Inhibit Type-I Interferon Signaling. Int. J. Mol. Sci. 2024, 25, 3753.
Choonnasard, A.; Shofa, M.; Okabayashi, T.; Saito, A. Conserved Functions of Orthohepadnavirus X Proteins to Inhibit Type-I Interferon Signaling. Int. J. Mol. Sci.2024, 25, 3753.
Choonnasard, A.; Shofa, M.; Okabayashi, T.; Saito, A. Conserved Functions of Orthohepadnavirus X Proteins to Inhibit Type-I Interferon Signaling. Int. J. Mol. Sci. 2024, 25, 3753.
Abstract
Orthohepadnavirus causes chronic hepatitis in a broad range of mammals, including primates, cats, woodchucks, and bats. Hepatitis B virus (HBV) X protein inhibits type-I interferon (IFN) signaling, promoting HBV escape from the innate immune system to establish persistent infection. However, whether X proteins of Orthohepadnavirus viruses in the other species have similar inhibitory activity remains unknown. Here, we investigated the anti-IFN activity of 17 Orthohepadnavirus X proteins derived from various hosts. We observed conserved activity of Orthohepadnavirus X proteins in inhibiting TIR-domain-containing adaptor protein inducing IFN-β (TRIF)-mediated IFN-β signaling pathway through TRIF degradation. X proteins from domestic cat hepadnavirus (DCH), a novel member of Orthohepadnavirus, inhibited mitochondrial antiviral signaling protein (MAVS)-mediated IFNβ signaling pathway comparable with HBV X. These results indicate that inhibition of IFN signaling is conserved in Orthohepadnavirus X proteins.
Keywords
Orthohepadnavirus, X protein, domestic cat hepadnavirus (DCH), hepatitis B virus (HBV), interferon-β signaling pathway
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
