Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68

DSpace/Manakin Repository

Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68

Show simple item record

dc.contributor.author E, Xiaofei
dc.contributor.author Hwang, Seungmin
dc.contributor.author Oh, Soohwan
dc.contributor.author Lee, Jong-Soo
dc.contributor.author Jeong, Joseph H.
dc.contributor.author Gwack, Yousang
dc.contributor.author Kowalik, Timothy F.
dc.contributor.author Sun, Ren
dc.contributor.author Liang, Chengyu
dc.contributor.author Stevenson, Philip G.
dc.contributor.author Jung, Jae Ung
dc.date.accessioned 2011-05-08T00:16:55Z
dc.date.issued 2009
dc.identifier.citation E, Xiaofei, Seungmin Hwang, Soohwan Oh, Jong-Soo Lee, Joseph H. Jeong, Yousang Gwack, Timothy F. Kowalik, Ren Sun, Jae U. Jung, and Chengyu Liang. 2009. Viral Bcl-2-mediated evasion of autophagy aids chronic infection of γHerpesvirus 68. PLoS Pathogens 5(10). en_US
dc.identifier.issn 1553-7366 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4882983
dc.description.abstract γ-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. en_US
dc.language.iso en_US en_US
dc.publisher Public Library of Science en_US
dc.relation.isversionof doi://10.1371/journal.ppat.1000609 en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752191/pdf/ en_US
dash.license LAA
dc.subject cell biology en_US
dc.subject microbiology en_US
dc.subject molecular biology en_US
dc.subject virology en_US
dc.title Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68 en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal PLoS Pathogens en_US
dash.depositing.author Jung, Jae Ung
dc.date.available 2011-05-08T00:16:55Z
dash.affiliation.other HMS^Microbiology and Molecular Genetics en_US

Files in this item

Files Size Format View
2752191.pdf 766.0Kb PDF View/Open

This item appears in the following Collection(s)

Show simple item record

 
 

Search DASH


Advanced Search
 
 

Submitters