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

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 i...

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Main Authors: Rachel Emily Levene, Marta Maria Gaglia
Format: Article
Language:English
Published: MDPI AG 2018-09-01
Series:Viruses
Subjects:
NS1
Online Access:http://www.mdpi.com/1999-4915/10/9/475
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spelling doaj-54be3c22e96e4032a2ef8821d3b8fde32020-11-24T22:20:07ZengMDPI AGViruses1999-49152018-09-0110947510.3390/v10090475v10090475Host Shutoff in Influenza A Virus: Many Means to an EndRachel Emily Levene0Marta Maria Gaglia1Graduate Program in Molecular Microbiology, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, MA 02111, USAGraduate Program in Molecular Microbiology, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, MA 02111, USAInfluenza 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.http://www.mdpi.com/1999-4915/10/9/475host shutoffPA-XNS1RNA-directed RNA polymeraseimmune evasioninfluenza
collection DOAJ
language English
format Article
sources DOAJ
author Rachel Emily Levene
Marta Maria Gaglia
spellingShingle Rachel Emily Levene
Marta Maria Gaglia
Host Shutoff in Influenza A Virus: Many Means to an End
Viruses
host shutoff
PA-X
NS1
RNA-directed RNA polymerase
immune evasion
influenza
author_facet Rachel Emily Levene
Marta Maria Gaglia
author_sort Rachel Emily Levene
title Host Shutoff in Influenza A Virus: Many Means to an End
title_short Host Shutoff in Influenza A Virus: Many Means to an End
title_full Host Shutoff in Influenza A Virus: Many Means to an End
title_fullStr Host Shutoff in Influenza A Virus: Many Means to an End
title_full_unstemmed Host Shutoff in Influenza A Virus: Many Means to an End
title_sort host shutoff in influenza a virus: many means to an end
publisher MDPI AG
series Viruses
issn 1999-4915
publishDate 2018-09-01
description 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.
topic host shutoff
PA-X
NS1
RNA-directed RNA polymerase
immune evasion
influenza
url http://www.mdpi.com/1999-4915/10/9/475
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