%0 Journal Article %A Paulmann, Dajana %A Magulski, Thomas %A Schwarz, Rebecca %A Heitmann, Lisa %A Flehmig, Bertram %A Vallbracht, Angelika %A Dotzauer, Andreas %T Hepatitis A virus protein 2B suppresses beta interferon (IFN) gene transcription by interfering with IFN regulatory factor 3 activation %D 2008 %J Journal of General Virology, %V 89 %N 7 %P 1593-1604 %@ 1465-2099 %R https://doi.org/10.1099/vir.0.83521-0 %I Microbiology Society, %X Hepatitis A virus (HAV) antagonizes the innate immune response by inhibition of retinoic acid-inducible gene I-mediated and melanoma differentiation-associated gene 5-mediated beta interferon (IFN-β) gene expression. This study showed that this is due to an interaction of HAV with mitochondrial antiviral signalling protein (MAVS)-dependent signalling, in which the viral non-structural protein 2B and the protein intermediate 3ABC recently suggested in this context seem to be involved, cooperatively affecting the activities of MAVS and the kinases TANK-binding kinase 1 (TBK1) and the inhibitor of NF-κB kinase ϵ (IKKϵ). In consequence, interferon regulatory factor 3 (IRF-3) is not activated. As IRF-3 is necessary for IFN-β transcription, inhibition of this factor results in efficient suppression of IFN-β synthesis. This ability might be of vital importance for HAV, which is an exceptionally slow growing virus sensitive to IFN-β, as it allows the virus to establish infection and maintain virus replication for a longer period of time. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.83521-0