Untersuchung und Identifizierung von Faktoren, die an der Hemmung der IFN-beta-Induktion bei einer Hepatitis A-Virusinfektion beteiligt sind

Abstract

Hepatitis A virus (HAV) antagonizes the innate immune response by inhibition of retinoic acid-inducible gene I (RIG-I)- and melanoma differentiation-associated gene 5 (MDA-5)-mediated interferon-beta gene expression. We show that this is due to an interaction of HAV with the signaling pathway component MAVS (mitochondrial antiviral signaling protein), in which the viral nonstructural protein 2B seems to be involved. In consequence, interferon regulatory factor 3 (IRF-3) is not activated. This resulzs in efficient suppression of IFN-beta synthesis.