Paramyxovirus evasion of innate immunity: Diverse strategies for common targets

Audsley, Michelle D.; Moseley, Gregory W.

doi:10.5501/wjv.v2.i2.57

Cited by 70 publications

(83 citation statements)

References 137 publications

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“…Most NSVs express a number of additional 'accessory' proteins, which are not essential for infection in vitro, but have been implicated in processes required for efficient replication and pathogenicity in vivo (Audsley & Moseley, 2013). Accessory proteins are encoded by genes additional to the usual genome complement, such as non-structural 1 and 2 proteins and short hydrophobic protein variously found in members of the Paramyxoviridae and a diverse array of accessory genes found in certain rhabdoviruses (Goodbourn & Randall, 2009;Walker et al, 2011), or are encoded as alternative products within conserved structural protein genes.…”

Section: The Infectious Cycle and Protein Coding Strategies Of Cytoplmentioning

confidence: 99%

“…Many paramyxovirus P genes also contain alternative open reading frames encoding one or more C proteins. A number of functions have been attributed to P-gene-encoded accessory proteins, but most commonly involve antagonism of the type I IFN-mediated innate immune response to viral infection [reviewed in Audsley & Moseley (2013) and in Ito et al (2016)]. …”

Section: The Infectious Cycle and Protein Coding Strategies Of Cytoplmentioning

confidence: 99%

“…Although structural proteins such as MeV N can inhibit IFN signalling, this aspect of infection by paramyxoviruses, lyssaviruses and other NSVs is mediated principally by accessory proteins (Audsley & Moseley, 2013;Ito et al, 2016). Type I IFN (IFN-a/b) induction (Fig.…”

Section: Genusmentioning

confidence: 99%

“…Nuclear NiV W binds and sequesters inactive (non-phosphorylated) STAT1/2 from the cytoplasm, preventing activation by JAKs; nuclear SeV Y1 inhibits ISG expression, by an undefined mechanism. A number of paramyxovirus V proteins interact with STAT1 and/or STAT2 in the cytoplasm, preventing signalling via various mechanisms including sequestration and degradation [see Audsley & Moseley (2013) for detailed review]. NiV, Nipah virus; SeV, Sendai virus; NPC, nuclear pore complex.…”

Section: Genusmentioning

confidence: 99%

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Roles of nuclear trafficking in infection by cytoplasmic negative-strand RNA viruses: paramyxoviruses and beyond

Audsley

Jans

Moseley

2016

Journal of General Virology

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Genome replication and virion production by most negative-sense RNA viruses (NSVs) occurs exclusively in the cytoplasm, but many NSV-expressed proteins undergo active nucleocytoplasmic trafficking via signals that exploit cellular nuclear transport pathways. Nuclear trafficking has been reported both for NSV accessory proteins (including isoforms of the rabies virus phosphoprotein, and V, W and C proteins of paramyxoviruses) and for structural proteins. Trafficking of the former is thought to enable accessory functions in viral modulation of antiviral responses including the type I IFN system, but the intranuclear roles of structural proteins such as nucleocapsid and matrix proteins, which have critical roles in extranuclear replication and viral assembly, are less clear. Nevertheless, nuclear trafficking of matrix protein has been reported to be critical for efficient production of Nipah virus and Respiratory syncytial virus, and nuclear localization of nucleocapsid protein of several morbilliviruses has been linked to mechanisms of immune evasion. Together, these data point to the nucleus as a significant host interface for viral proteins during infection by NSVs with otherwise cytoplasmic life cycles. Importantly, several lines of evidence now suggest that nuclear trafficking of these proteins may be critical to pathogenesis and thus could provide new targets for vaccine development and antiviral therapies.

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Section: The Infectious Cycle and Protein Coding Strategies Of Cytoplmentioning

confidence: 99%

Section: The Infectious Cycle and Protein Coding Strategies Of Cytoplmentioning

confidence: 99%

Section: Genusmentioning

confidence: 99%

Section: Genusmentioning

confidence: 99%

See 2 more Smart Citations

Roles of nuclear trafficking in infection by cytoplasmic negative-strand RNA viruses: paramyxoviruses and beyond

Audsley

Jans

Moseley

2016

Journal of General Virology

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“…The relationship between viruses and the host cell defensive system is the particular focus of the two following reviews "Innate host responses to West Nile virus: Implications for central nervous system immunopathology", by Rossini et al [3] and "Paramyxovirus evasion of innate immunity: Diverse strategies for common targets" by Audsley et al [4] , which both provide a simultaneously accurate and concise summary of viral strategies to subvert the innate response at the molecular level, and the implication thereof in viral mediated pathogenesis.…”

Section: Editorialmentioning

confidence: 99%

Reprogramming the host: Modification of cell functions upon viral infection

Alvisi¹

2013

WJV

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Viruses and their hosts have co-evolved for million years. In order to successfully replicate their genome, viruses need to usurp the biosynthetic machinery of the host cell. Depending on the complexity and the nature of the genome, replication might involve or not a relatively large subset of viral products, in addition to a number of host cell factors, and take place in several subcellular compartments, including the nucleus, the cytoplasm, as well as virus-induced, rearranged membranes. Therefore viruses need to ensure the correct subcellular localization of their effectors and to be capable of disguising from the cellular defensive mechanisms. In addition, viruses are capable of exploiting host cell activities, by modulating their post-translational modification apparatus, resulting in profound modifications in the function of cellular and viral products. Not surprisingly infection of host cells by these parasites can lead to alterations of cellular differentiation and growing properties, with important pathogenic consequences. In the present hot topic highlight entitled "Reprogramming the host: modification of cell functions upon viral infection", a number of leading virologists and cell biologist thoroughly describe recent advances in our understanding of how viruses modulate cellular functions to achieve successful replication and propagation at the expenses of human cells.© 2013 Baishideng. All rights reserved.Key words: Virus-host interaction; Pathogenesis; Post translational modification; Viral factories; Cancer; Differentiation; Human immunodeficiency virus; Hepatitis C virus; RNAi Core tip: Viruses are obliged intracellular parasites causing million causalities every year. In order to successfully replicate their genome, viruses need to usurp the biosynthetic machinery of the host cell. Depending on the complexity and the nature of the genome, replication might involve or not a relatively large subset of viral products, in addition to a number of host cell factors, and take place in several subcellular compartments, including the nucleus, the cytoplasm, as well as virusinduced, rearranged membranes. We describe recent advances in our understanding of how viruses modulate cellular functions to successfully replicate at the expenses of human cells. Viruses and their hosts have co-evolved for million years. In order to successfully replicate their genome, viruses need to usurp the biosynthetic machinery of the host cell. Depending on the complexity and the nature of the genome, replication might involve or not a relatively large subset of viral products, in addition to a number of host cell factors, and take place in several subcellular compartments, including the nucleus, the cytoplasm, as well as virus-induced, rearranged membranes. Therefore viruses need to ensure the correct subcellular localization of their effectors and to be capable of disguising from the cellular defensive mechanisms. In this hot topic highlight entitled "Reprogramming the host: Modification of cell functions upon viral ...

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Antiviral Effects of Inhibiting Host Gene Expression

Tripp

Tompkins

2014

Current Topics in Microbiology and Immunology

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RNA interference (RNAi) has been used to probe the virus-host interface to understand the requirements for host-gene expression needed for virus replication. The availability of arrayed siRNA libraries has enabled a genome-scale, high-throughput analysis of gene pathways usurped for virus replication. Results from these and related screens have led to the discovery of new host factors that regulate virus replication. While effective delivery continues to limit development of RNAi-based drugs, RNAi-based genome discovery has led to identification of druggable targets. These validated targets enable rational development of novel antiviral drugs, including the rescue and repurposing of existing, approved drugs. Existing drugs with known cytotoxicity and mechanisms of action can potentially be re-targeted to regulate host genes and gene products needed by influenza to replicate. Drug repositioning is more cost-effective, less time-consuming, and more effective for anti-influenza virus drug discovery than traditional methods. In this chapter, a general overview of RNAi screening methods, host-gene discovery, and drug repurposing is examined with emphasis on utilizing RNAi to identify druggable genes that can be targeted for drug development or repurposing.

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Paramyxovirus evasion of innate immunity: Diverse strategies for common targets

Cited by 70 publications

References 137 publications

Roles of nuclear trafficking in infection by cytoplasmic negative-strand RNA viruses: paramyxoviruses and beyond

Roles of nuclear trafficking in infection by cytoplasmic negative-strand RNA viruses: paramyxoviruses and beyond

Reprogramming the host: Modification of cell functions upon viral infection

Antiviral Effects of Inhibiting Host Gene Expression

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