The immune evasion function of J and Beilong virus V proteins is distinct from that of other paramyxoviruses, consistent with their inclusion in the proposed genus Jeilongvirus

Michelle D. Audsley, Glenn A. Marsh, Kim G. Lieu, Mary Tachedjian, D. Albert Joubert, Lin-Fa Wang, David A. Jans, Gregory W. Moseley

Research output: Contribution to journalArticleResearchpeer-review

11 Citations (Scopus)

Abstract

IFN-antagonist function is a major determinant of pathogenicity and cross-species infection by viruses, but remains poorly defined for many potentially zoonotic viruses resident in animal species. The paramyxovirus family contains several zoonotic viruses, including highly pathogenic viruses such as Nipah virus and Hendra virus, and an increasing number of largely uncharacterized animal viruses. Here, we report the characterization of IFN antagonism by the rodent viruses J virus (JPV) and Beilong virus (BeiPV) of the proposed genus Jeilongvirus of the paramyxoviruses. Infection of cells by JPV and BeiPV was found to inhibit IFN-activated nuclear translocation of signal transducer and activator of transcription 1 (STAT1). However, in contrast to most other paramyxoviruses, the JPV and BeiPV V proteins did not interact with or inhibit signalling by STAT1 or STAT2, suggesting that JPV/BeiPV use an atypical V protein-independent strategy to target STATs, consistent with their inclusion in a separate genus. Nevertheless, the V proteins of both viruses interacted with melanoma differentiation-associated protein 5 (MDA5) and robustly inhibited MDA5-dependent activation of the IFN-β promoter. This supports a growing body of evidence that MDA5 is a universal target of paramyxovirus V proteins, such that the V–MDA5 interaction represents a potential target for broad-spectrum antiviral approaches.
Original languageEnglish
Pages (from-to)581-592
Number of pages12
JournalJournal of General Virology
Volume97
Issue number3
DOIs
Publication statusPublished - Mar 2016

Cite this

@article{8c603405d68640819a398cf196edd4eb,
title = "The immune evasion function of J and Beilong virus V proteins is distinct from that of other paramyxoviruses, consistent with their inclusion in the proposed genus Jeilongvirus",
abstract = "IFN-antagonist function is a major determinant of pathogenicity and cross-species infection by viruses, but remains poorly defined for many potentially zoonotic viruses resident in animal species. The paramyxovirus family contains several zoonotic viruses, including highly pathogenic viruses such as Nipah virus and Hendra virus, and an increasing number of largely uncharacterized animal viruses. Here, we report the characterization of IFN antagonism by the rodent viruses J virus (JPV) and Beilong virus (BeiPV) of the proposed genus Jeilongvirus of the paramyxoviruses. Infection of cells by JPV and BeiPV was found to inhibit IFN-activated nuclear translocation of signal transducer and activator of transcription 1 (STAT1). However, in contrast to most other paramyxoviruses, the JPV and BeiPV V proteins did not interact with or inhibit signalling by STAT1 or STAT2, suggesting that JPV/BeiPV use an atypical V protein-independent strategy to target STATs, consistent with their inclusion in a separate genus. Nevertheless, the V proteins of both viruses interacted with melanoma differentiation-associated protein 5 (MDA5) and robustly inhibited MDA5-dependent activation of the IFN-β promoter. This supports a growing body of evidence that MDA5 is a universal target of paramyxovirus V proteins, such that the V–MDA5 interaction represents a potential target for broad-spectrum antiviral approaches.",
author = "Audsley, {Michelle D.} and Marsh, {Glenn A.} and Lieu, {Kim G.} and Mary Tachedjian and Joubert, {D. Albert} and Lin-Fa Wang and Jans, {David A.} and Moseley, {Gregory W.}",
year = "2016",
month = "3",
doi = "10.1099/jgv.0.000388",
language = "English",
volume = "97",
pages = "581--592",
journal = "Journal of General Virology",
issn = "0022-1317",
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}

The immune evasion function of J and Beilong virus V proteins is distinct from that of other paramyxoviruses, consistent with their inclusion in the proposed genus Jeilongvirus. / Audsley, Michelle D.; Marsh, Glenn A.; Lieu, Kim G.; Tachedjian, Mary; Joubert, D. Albert; Wang, Lin-Fa; Jans, David A.; Moseley, Gregory W.

In: Journal of General Virology, Vol. 97, No. 3, 03.2016, p. 581-592.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - The immune evasion function of J and Beilong virus V proteins is distinct from that of other paramyxoviruses, consistent with their inclusion in the proposed genus Jeilongvirus

AU - Audsley, Michelle D.

AU - Marsh, Glenn A.

AU - Lieu, Kim G.

AU - Tachedjian, Mary

AU - Joubert, D. Albert

AU - Wang, Lin-Fa

AU - Jans, David A.

AU - Moseley, Gregory W.

PY - 2016/3

Y1 - 2016/3

N2 - IFN-antagonist function is a major determinant of pathogenicity and cross-species infection by viruses, but remains poorly defined for many potentially zoonotic viruses resident in animal species. The paramyxovirus family contains several zoonotic viruses, including highly pathogenic viruses such as Nipah virus and Hendra virus, and an increasing number of largely uncharacterized animal viruses. Here, we report the characterization of IFN antagonism by the rodent viruses J virus (JPV) and Beilong virus (BeiPV) of the proposed genus Jeilongvirus of the paramyxoviruses. Infection of cells by JPV and BeiPV was found to inhibit IFN-activated nuclear translocation of signal transducer and activator of transcription 1 (STAT1). However, in contrast to most other paramyxoviruses, the JPV and BeiPV V proteins did not interact with or inhibit signalling by STAT1 or STAT2, suggesting that JPV/BeiPV use an atypical V protein-independent strategy to target STATs, consistent with their inclusion in a separate genus. Nevertheless, the V proteins of both viruses interacted with melanoma differentiation-associated protein 5 (MDA5) and robustly inhibited MDA5-dependent activation of the IFN-β promoter. This supports a growing body of evidence that MDA5 is a universal target of paramyxovirus V proteins, such that the V–MDA5 interaction represents a potential target for broad-spectrum antiviral approaches.

AB - IFN-antagonist function is a major determinant of pathogenicity and cross-species infection by viruses, but remains poorly defined for many potentially zoonotic viruses resident in animal species. The paramyxovirus family contains several zoonotic viruses, including highly pathogenic viruses such as Nipah virus and Hendra virus, and an increasing number of largely uncharacterized animal viruses. Here, we report the characterization of IFN antagonism by the rodent viruses J virus (JPV) and Beilong virus (BeiPV) of the proposed genus Jeilongvirus of the paramyxoviruses. Infection of cells by JPV and BeiPV was found to inhibit IFN-activated nuclear translocation of signal transducer and activator of transcription 1 (STAT1). However, in contrast to most other paramyxoviruses, the JPV and BeiPV V proteins did not interact with or inhibit signalling by STAT1 or STAT2, suggesting that JPV/BeiPV use an atypical V protein-independent strategy to target STATs, consistent with their inclusion in a separate genus. Nevertheless, the V proteins of both viruses interacted with melanoma differentiation-associated protein 5 (MDA5) and robustly inhibited MDA5-dependent activation of the IFN-β promoter. This supports a growing body of evidence that MDA5 is a universal target of paramyxovirus V proteins, such that the V–MDA5 interaction represents a potential target for broad-spectrum antiviral approaches.

UR - http://www.ncbi.nlm.nih.gov/pubmed/26703878

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DO - 10.1099/jgv.0.000388

M3 - Article

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SP - 581

EP - 592

JO - Journal of General Virology

JF - Journal of General Virology

SN - 0022-1317

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ER -