Host translation shutoff mediated by non-structural protein 2 is a critical factor in the antiviral state resistance of Venezuelan equine encephalitis virus
Abstract Most previous studies of interferon-alpha/beta (IFN-α/β) response antagonism by alphaviruses have focused upon interruption of IFN-α/β induction and/or receptor signaling cascades. Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum...
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| Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2016-09, Vol.496, p.147-165 |
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| creator | Bhalla, Nishank Sun, Chengqun Metthew Lam, L.K Gardner, Christina L Ryman, Kate D Klimstra, William B |
| description | Abstract Most previous studies of interferon-alpha/beta (IFN-α/β) response antagonism by alphaviruses have focused upon interruption of IFN-α/β induction and/or receptor signaling cascades. Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum IFN-α/β, that elicits a systemic antiviral state in uninfected cells successfully controlling SINV but not VEEV replication. Furthermore, VEEV replication is more resistant than that of SINV to a pre-existing antiviral state in vitro . While host macromolecular shutoff is proposed as a major antagonist of IFN-α/β induction, the underlying mechanisms of alphavirus resistance to a pre-existing antiviral state are not fully defined, nor is the mechanism for the greater resistance of VEEV. Here, we have separated viral transcription and translation shutoff with multiple alphaviruses, identified the viral proteins that induce each activity, and demonstrated that VEEV nonstructural protein 2-induced translation shutoff is likely a critical factor in enhanced antiviral state resistance of this alphavirus. |
| doi_str_mv | 10.1016/j.virol.2016.06.005 |
| format | Article |
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Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum IFN-α/β, that elicits a systemic antiviral state in uninfected cells successfully controlling SINV but not VEEV replication. Furthermore, VEEV replication is more resistant than that of SINV to a pre-existing antiviral state in vitro . While host macromolecular shutoff is proposed as a major antagonist of IFN-α/β induction, the underlying mechanisms of alphavirus resistance to a pre-existing antiviral state are not fully defined, nor is the mechanism for the greater resistance of VEEV. Here, we have separated viral transcription and translation shutoff with multiple alphaviruses, identified the viral proteins that induce each activity, and demonstrated that VEEV nonstructural protein 2-induced translation shutoff is likely a critical factor in enhanced antiviral state resistance of this alphavirus.</description><identifier>ISSN: 0042-6822</identifier><identifier>ISSN: 1096-0341</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/j.virol.2016.06.005</identifier><identifier>PMID: 27318152</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alphavirus ; Animals ; Antiviral Agents - metabolism ; Antiviral Agents - pharmacology ; Antiviral state resistance ; Cell Line ; Chikungunya virus ; Disease Resistance ; Eastern equine encephalitis virus ; Encephalitis Virus, Venezuelan Equine - drug effects ; Encephalitis Virus, Venezuelan Equine - physiology ; Encephalomyelitis, Venezuelan Equine - genetics ; Encephalomyelitis, Venezuelan Equine - metabolism ; Encephalomyelitis, Venezuelan Equine - mortality ; Encephalomyelitis, Venezuelan Equine - virology ; Horses ; Host-Pathogen Interactions ; Humans ; Infectious Disease ; Interferon ; Interferons - biosynthesis ; Interferons - pharmacology ; Mice ; Mutation ; Nonstructural protein 2 ; Phenotype ; Protein Biosynthesis ; RNA, Viral ; Sindbis virus ; Transcription shutoff ; Translation shutoff ; Venezuelan equine encephalitis virus ; Viral Nonstructural Proteins - genetics ; Viral Nonstructural Proteins - metabolism</subject><ispartof>Virology (New York, N.Y.), 2016-09, Vol.496, p.147-165</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. 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Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum IFN-α/β, that elicits a systemic antiviral state in uninfected cells successfully controlling SINV but not VEEV replication. Furthermore, VEEV replication is more resistant than that of SINV to a pre-existing antiviral state in vitro . While host macromolecular shutoff is proposed as a major antagonist of IFN-α/β induction, the underlying mechanisms of alphavirus resistance to a pre-existing antiviral state are not fully defined, nor is the mechanism for the greater resistance of VEEV. Here, we have separated viral transcription and translation shutoff with multiple alphaviruses, identified the viral proteins that induce each activity, and demonstrated that VEEV nonstructural protein 2-induced translation shutoff is likely a critical factor in enhanced antiviral state resistance of this alphavirus.</description><subject>Alphavirus</subject><subject>Animals</subject><subject>Antiviral Agents - metabolism</subject><subject>Antiviral Agents - pharmacology</subject><subject>Antiviral state resistance</subject><subject>Cell Line</subject><subject>Chikungunya virus</subject><subject>Disease Resistance</subject><subject>Eastern equine encephalitis virus</subject><subject>Encephalitis Virus, Venezuelan Equine - drug effects</subject><subject>Encephalitis Virus, Venezuelan Equine - physiology</subject><subject>Encephalomyelitis, Venezuelan Equine - genetics</subject><subject>Encephalomyelitis, Venezuelan Equine - metabolism</subject><subject>Encephalomyelitis, Venezuelan Equine - mortality</subject><subject>Encephalomyelitis, Venezuelan Equine - virology</subject><subject>Horses</subject><subject>Host-Pathogen Interactions</subject><subject>Humans</subject><subject>Infectious Disease</subject><subject>Interferon</subject><subject>Interferons - biosynthesis</subject><subject>Interferons - pharmacology</subject><subject>Mice</subject><subject>Mutation</subject><subject>Nonstructural protein 2</subject><subject>Phenotype</subject><subject>Protein Biosynthesis</subject><subject>RNA, Viral</subject><subject>Sindbis virus</subject><subject>Transcription shutoff</subject><subject>Translation shutoff</subject><subject>Venezuelan equine encephalitis virus</subject><subject>Viral Nonstructural Proteins - genetics</subject><subject>Viral Nonstructural Proteins - metabolism</subject><issn>0042-6822</issn><issn>1096-0341</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUk2LFDEQbURxx9VfIEiOXnrMR6e7c3BBltUVFjz4cQ3pdMXJ2JPMJumB8bf4Y6121kW9CAVJpd57SepVVT1ndM0oa19t1wef4rTmmKwpBpUPqhWjqq2paNjDakVpw-u25_ysepLzlmLedfRxdcY7wXom-ar6cR1zISWZkCdTfAwkb-YSnSM7GL0pMJLhSEIMdS5ptmVOZiL7FAv4QDjxmRhiky_e4rkztsREsFI2QEwoHl-I57mgEEmQPe6CBRId-QIBvs8wmUDgdvYBCGBlvzETimWCxDk_rR45M2V4dreeV5_fXn26vK5vPrx7f_nmpraSNaXulWtgkIIrZaRhphPWGcFGpVjHDOtMo0Q7KtEZGJwTQkEvZd9zqphTYzOI8-ripLufB_y2hYANmfQ--Z1JRx2N139Xgt_or_GgZc8Zoz0KvLwTSPF2hlz0zmcLE_4O4pw16xHUyZ5ShIoT1KaYcwJ3fw2jevFVb_UvX_Xiq6YYVCLrxZ8vvOf8NhIBr08AwD4dPCSdrV86OvoEtugx-v9ccPEP304-LK5-gyPkbZxTQAs005lrqj8uo7VMFmsFZU0rxU_e1s8J</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Bhalla, Nishank</creator><creator>Sun, Chengqun</creator><creator>Metthew Lam, L.K</creator><creator>Gardner, Christina L</creator><creator>Ryman, Kate D</creator><creator>Klimstra, William B</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160901</creationdate><title>Host translation shutoff mediated by non-structural protein 2 is a critical factor in the antiviral state resistance of Venezuelan equine encephalitis virus</title><author>Bhalla, Nishank ; Sun, Chengqun ; Metthew Lam, L.K ; Gardner, Christina L ; Ryman, Kate D ; Klimstra, William B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-89f4eb53299a5a1a73cfa31d99171a17a4936d937aebff339e855882091f9d4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alphavirus</topic><topic>Animals</topic><topic>Antiviral Agents - metabolism</topic><topic>Antiviral Agents - pharmacology</topic><topic>Antiviral state resistance</topic><topic>Cell Line</topic><topic>Chikungunya virus</topic><topic>Disease Resistance</topic><topic>Eastern equine encephalitis virus</topic><topic>Encephalitis Virus, Venezuelan Equine - drug effects</topic><topic>Encephalitis Virus, Venezuelan Equine - physiology</topic><topic>Encephalomyelitis, Venezuelan Equine - genetics</topic><topic>Encephalomyelitis, Venezuelan Equine - metabolism</topic><topic>Encephalomyelitis, Venezuelan Equine - mortality</topic><topic>Encephalomyelitis, Venezuelan Equine - virology</topic><topic>Horses</topic><topic>Host-Pathogen Interactions</topic><topic>Humans</topic><topic>Infectious Disease</topic><topic>Interferon</topic><topic>Interferons - biosynthesis</topic><topic>Interferons - pharmacology</topic><topic>Mice</topic><topic>Mutation</topic><topic>Nonstructural protein 2</topic><topic>Phenotype</topic><topic>Protein Biosynthesis</topic><topic>RNA, Viral</topic><topic>Sindbis virus</topic><topic>Transcription shutoff</topic><topic>Translation shutoff</topic><topic>Venezuelan equine encephalitis virus</topic><topic>Viral Nonstructural Proteins - genetics</topic><topic>Viral Nonstructural Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bhalla, Nishank</creatorcontrib><creatorcontrib>Sun, Chengqun</creatorcontrib><creatorcontrib>Metthew Lam, L.K</creatorcontrib><creatorcontrib>Gardner, Christina L</creatorcontrib><creatorcontrib>Ryman, Kate D</creatorcontrib><creatorcontrib>Klimstra, William B</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bhalla, Nishank</au><au>Sun, Chengqun</au><au>Metthew Lam, L.K</au><au>Gardner, Christina L</au><au>Ryman, Kate D</au><au>Klimstra, William B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Host translation shutoff mediated by non-structural protein 2 is a critical factor in the antiviral state resistance of Venezuelan equine encephalitis virus</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>496</volume><spage>147</spage><epage>165</epage><pages>147-165</pages><issn>0042-6822</issn><issn>1096-0341</issn><eissn>1096-0341</eissn><abstract>Abstract Most previous studies of interferon-alpha/beta (IFN-α/β) response antagonism by alphaviruses have focused upon interruption of IFN-α/β induction and/or receptor signaling cascades. Infection of mice with Venezuelan equine encephalitis alphavirus (VEEV) or Sindbis virus (SINV) induces serum IFN-α/β, that elicits a systemic antiviral state in uninfected cells successfully controlling SINV but not VEEV replication. Furthermore, VEEV replication is more resistant than that of SINV to a pre-existing antiviral state in vitro . While host macromolecular shutoff is proposed as a major antagonist of IFN-α/β induction, the underlying mechanisms of alphavirus resistance to a pre-existing antiviral state are not fully defined, nor is the mechanism for the greater resistance of VEEV. 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| identifier | ISSN: 0042-6822 |
| ispartof | Virology (New York, N.Y.), 2016-09, Vol.496, p.147-165 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier); EZB Electronic Journals Library |
| subjects | Alphavirus Animals Antiviral Agents - metabolism Antiviral Agents - pharmacology Antiviral state resistance Cell Line Chikungunya virus Disease Resistance Eastern equine encephalitis virus Encephalitis Virus, Venezuelan Equine - drug effects Encephalitis Virus, Venezuelan Equine - physiology Encephalomyelitis, Venezuelan Equine - genetics Encephalomyelitis, Venezuelan Equine - metabolism Encephalomyelitis, Venezuelan Equine - mortality Encephalomyelitis, Venezuelan Equine - virology Horses Host-Pathogen Interactions Humans Infectious Disease Interferon Interferons - biosynthesis Interferons - pharmacology Mice Mutation Nonstructural protein 2 Phenotype Protein Biosynthesis RNA, Viral Sindbis virus Transcription shutoff Translation shutoff Venezuelan equine encephalitis virus Viral Nonstructural Proteins - genetics Viral Nonstructural Proteins - metabolism |
| title | Host translation shutoff mediated by non-structural protein 2 is a critical factor in the antiviral state resistance of Venezuelan equine encephalitis virus |
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