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Article: Viral Bcl-2-mediated evasion of autophagy aids chronic infection of γherpesvirus 68

TitleViral Bcl-2-mediated evasion of autophagy aids chronic infection of γherpesvirus 68
Authors
Issue Date2009
Citation
PLoS Pathogens, 2009, v. 5, n. 10, article no. e1000609 How to Cite?
Abstractγ-herpesviruses (γHVs) have developed an interaction with their hosts wherein they establish a life-long persistent infection and are associated with the onset of various malignancies. One critical virulence factor involved in the persistency of murine γ-herpesvirus 68 (γHV68) is the viral homolog of the Bcl-2 protein (vBcl-2), which has been implicated to counteract both host apoptotic responses and autophagy pathway. However, the relative significance of the two activities of vBcl-2 in viral persistent infection has yet to be elucidated. Here, by characterizing a series of loss-of-function mutants of vBcl-2, we have distinguished the vBcl-2-mediated antagonism of autophagy from the vBcl-2-mediated inhibition of apoptosis in vitro and in vivo. A mutant γHV68 virus lacking the anti-autophagic activity of vBcl-2 demonstrates an impaired ability to maintain chronic infections in mice, whereas a mutant virus lacking the anti-apoptotic activity of vBcl-2 establishes chronic infections as efficiently as the wild-type virus but displays a compromised ability for ex vivo reactivation. Thus, the vBcl-2-mediated antagonism of host autophagy constitutes a novel mechanism by which γHVs confer persistent infections, further underscoring the importance of autophagy as a critical host determinant in the in vivo latency of γ-herpesviruses. © 2009 E et al.
Persistent Identifierhttp://hdl.handle.net/10722/285659
ISSN
2023 Impact Factor: 5.5
2023 SCImago Journal Rankings: 2.223
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorE, Xiaofei-
dc.contributor.authorHwang, Seungmin-
dc.contributor.authorOh, Soohwan-
dc.contributor.authorLee, Jong Soo-
dc.contributor.authorJeong, Joseph H.-
dc.contributor.authorGwack, Yousang-
dc.contributor.authorKowalik, Timothy F.-
dc.contributor.authorSun, Ren-
dc.contributor.authorJung, Jae U.-
dc.contributor.authorLiang, Chengyu-
dc.date.accessioned2020-08-18T04:56:19Z-
dc.date.available2020-08-18T04:56:19Z-
dc.date.issued2009-
dc.identifier.citationPLoS Pathogens, 2009, v. 5, n. 10, article no. e1000609-
dc.identifier.issn1553-7366-
dc.identifier.urihttp://hdl.handle.net/10722/285659-
dc.description.abstractγ-herpesviruses (γHVs) have developed an interaction with their hosts wherein they establish a life-long persistent infection and are associated with the onset of various malignancies. One critical virulence factor involved in the persistency of murine γ-herpesvirus 68 (γHV68) is the viral homolog of the Bcl-2 protein (vBcl-2), which has been implicated to counteract both host apoptotic responses and autophagy pathway. However, the relative significance of the two activities of vBcl-2 in viral persistent infection has yet to be elucidated. Here, by characterizing a series of loss-of-function mutants of vBcl-2, we have distinguished the vBcl-2-mediated antagonism of autophagy from the vBcl-2-mediated inhibition of apoptosis in vitro and in vivo. A mutant γHV68 virus lacking the anti-autophagic activity of vBcl-2 demonstrates an impaired ability to maintain chronic infections in mice, whereas a mutant virus lacking the anti-apoptotic activity of vBcl-2 establishes chronic infections as efficiently as the wild-type virus but displays a compromised ability for ex vivo reactivation. Thus, the vBcl-2-mediated antagonism of host autophagy constitutes a novel mechanism by which γHVs confer persistent infections, further underscoring the importance of autophagy as a critical host determinant in the in vivo latency of γ-herpesviruses. © 2009 E et al.-
dc.languageeng-
dc.relation.ispartofPLoS Pathogens-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleViral Bcl-2-mediated evasion of autophagy aids chronic infection of γherpesvirus 68-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.ppat.1000609-
dc.identifier.pmid19816569-
dc.identifier.pmcidPMC2752191-
dc.identifier.scopuseid_2-s2.0-73649092138-
dc.identifier.volume5-
dc.identifier.issue10-
dc.identifier.spagearticle no. e1000609-
dc.identifier.epagearticle no. e1000609-
dc.identifier.eissn1553-7374-
dc.identifier.isiWOS:000272033300014-
dc.identifier.issnl1553-7366-

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