Influenza A virus replication is dependent on an antioxidant pathway that involves GSH and Bcl-2.

Lucia Nencioni, Alessandra Iuvara, Katia Aquilano, Maria R. Ciriolo, Federico Cozzolino, Giuseppe Rotilio, Enrico Garaci, Anna T. Palamara

Research output: Contribution to journalArticlepeer-review

Abstract

Growing evidence indicates that viral replication is regulated by the redox state of the host cell. We demonstrate that cells of different origins display differential permissivity for influenza A virus replication, depending on their intracellular redox power as reflected by Bcl-2 expression and glutathione (GSH) content. Bcl-2 expressing cells were found to have higher intracellular levels of GSH and to produce lower amounts of virus than Bcl-2 negative cells. Two different steps in the virus life-cycle were involved in Bcl-2/GSH mediated viral inhibition: 1) expression of late viral proteins (in particular hemagglutinin and matrix); and 2) nuclear-cytoplasmic translocation of viral ribonucleoproteins (vRNPs). Buthionine-sulfoximine-induced inhibition of GSH synthesis in Bcl-2 expressing cells caused an increase in the expression of late viral proteins but did not restore vRNP export to the cytoplasm. Collectively, our findings show that both Bcl-2 expression and GSH content contribute to the host cell's ability to down-regulate influenza virus replication, although their effects are exerted at different stages of the viral life-cycle. In certain cell populations, this form of down-regulation might conceivably favor the establishment of persistent viral infection.

Original languageEnglish
Pages (from-to)758-760
Number of pages3
JournalFASEB Journal
Volume17
Issue number6
Publication statusPublished - 2003

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