Influenza exits the cell without an ESCRT.

Program in Gene Function and Expression, Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Cell (Impact Factor: 32.24). 09/2010; 142(6):839-41. DOI: 10.1016/j.cell.2010.08.036
Source: PubMed


Many enveloped viruses depend on the membrane remodeling machinery of their host cells to complete their life cycle. In this issue, Rossman et al. (2010) now demonstrate that influenza virus possesses its own device for releasing nascent virus particles from the plasma membrane, the M2 proton-selective ion channel, which can substitute for the host cell's ESCRT pathway.

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Available from: Heinrich G Gottlinger, Aug 24, 2015
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    ABSTRACT: Caveolin expression supports the multiplication of retro-, ortho- and paramyxoviruses in susceptible cells. However, human influenza A virus (IAV), an orthomyxovirus, does not multiply efficiently in mouse embryo fibroblasts (MEFs), which are abundant in caveolin-1 (Cav-1). Surprisingly, the absence of Cav-1 in a MEF cell line removed the block for IAV replication and raised the infectious titer 250-fold, whereas the re-introduction of Cav-1 reversed the effect. The monitoring of cellular pathways revealed that Cav-1 loss considerably increased activities of p53. Furthermore, infection of MEF Cav-1 (-/-) induced reactive oxygen species (ROS) and pronounced apoptosis in the late phase of viral multiplication, but no type I IFN response. Strikingly, pharmacological inactivation showed that the elevated levels of ROS together with apoptosis caused the increase of virus yield. Thus, Cav-1 represents a new negative regulator of IAV infection in MEF that diminishes IAV infectious titer by controlling virus-supportive pathways.
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