作者: Marguerite Kreit , Didier Vertommen , Laurent Gillet , Thomas Michiels
DOI: 10.1371/JOURNAL.PONE.0133190
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摘要: Apolipoprotein L9b (Apol9b) is an interferon-stimulated gene (ISG) that has antiviral activity and weakly expressed in primary mouse neurons as compared to other cell types. Here, we show both Apol9 isoforms (Apol9b Apol9a) inhibit replication of Theiler’s murine encephalomyelitis virus (TMEV) but not vesicular stomatitis (VSV), Murid herpesvirus-4 (MuHV-4), or infection by a lentiviral vector. genes are strongly liver and, lesser extent, pancreas, adipose tissue intestine. Their expression increased type I interferon viral infection. In contrast genuine apolipoproteins involved lipid transport, ApoL9 intracytoplasmic localization does seem be secreted. The cytoplasmic line with the observation inhibits step TMEV human ApoL6, did sensitize cells apoptosis, spite presence conserved putative BH3 domain, required for activity. ApoL9a b interact cellular prohibitin 1 (Phb1) 2 (Phb2) this interaction might contribute Knocking down Phb2 slightly replication, irrespective overexpression. prohibitins against contrasts pro-viral observed VSV reported previously Dengue (DENV-2), Chikungunya (CHIKV) influenza H5N1 viruses. thus example ISG displaying narrow range, which likely acts complex restrict replication.