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Host Shutoff in Influenza A Virus: Many Means to an End

tetano

Editor, Senior Moderator
Viruses. 2018 Sep 5;10(9). pii: E475. doi: 10.3390/v10090475.
[h=1]Host Shutoff in Influenza A Virus: Many Means to an End.[/h] Levene RE[SUP]1,[/SUP][SUP]2[/SUP], Gaglia MM[SUP]3,[/SUP][SUP]4[/SUP].
[h=3]Author information[/h]

[h=3]Abstract[/h] Influenza A virus carries few of its own proteins, but uses them effectively to take control of the infected cells and avoid immune responses. Over the years, host shutoff, the widespread down-regulation of host gene expression, has emerged as a key process that contributes to cellular takeover in infected cells. Interestingly, multiple mechanisms of host shutoff have been described in influenza A virus, involving changes in translation, RNA synthesis and stability. Several viral proteins, notably the non-structural protein NS1, the RNA-dependent RNA polymerase and the endoribonuclease PA-X have been implicated in host shutoff. This multitude of host shutoff mechanisms indicates that host shutoff is an important component of the influenza A virus replication cycle. Here we review the various mechanisms of host shutoff in influenza A virus and the evidence that they contribute to immune evasion and/or viral replication. We also discuss what the purpose of having multiple mechanisms may be.


[h=4]KEYWORDS:[/h] NS1; PA-X; RNA-directed RNA polymerase; host shutoff; immune evasion; influenza

PMID: 30189604 DOI: 10.3390/v10090475
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