Journal of virology · 2012
The PI3K/Akt pathway contributes to arenavirus budding.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Urata Shuzo, Ngo Nhi, de la Torre Juan Carlos
Аннотация
Several arenaviruses, chiefly Lassa virus (LASV), cause hemorrhagic fever (HF) disease in humans and pose a significant public health concern in regions where they are endemic. On the other hand, evidence indicates that the globally distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway participates in many cellular processes, including cell survival and differentiation, and also has been shown to play important roles in different steps of the life cycles of a variety of viruses. Here we report that the inhibition of the PI3K/Akt pathway inhibited budding and to a lesser extent RNA synthesis, but not cell entry, of LCMV. Accordingly, BEZ-235, a PI3K inhibitor currently in cancer clinical trials, inhibited LCMV multiplication in cultured cells. These findings, together with those previously reported for Junin virus (JUNV), indicate that targeting the PI3K/Akt pathway could represent a novel antiviral strategy to combat human-pathogenic arenaviruses.
Предметные рубрики MeSH
AnimalsArenavirusCell LineChlorocebus aethiopsChromonesGene Expression Regulation, ViralHumansImidazolesLassa virusLymphocytic choriomeningitis virusMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktQuinolinesRNA, ViralSignal TransductionSirolimusVirus InternalizationVirus ReleaseVirus Replication