Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68
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Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68
| Title: | Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of γHerpesvirus 68 |
| Author: |
E, Xiaofei; Hwang, Seungmin; Oh, Soohwan; Lee, Jong-Soo; Jeong, Joseph H.; Gwack, Yousang; Kowalik, Timothy F.; Sun, Ren; Liang, Chengyu; Stevenson, Philip G.; Jung, Jae Ung
Note: Order does not necessarily reflect citation order of authors. |
| 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). |
| Full Text & Related Files: |
2752191.pdf (784.3Kb; PDF) 
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| 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. |
| Published Version: | doi://10.1371/journal.ppat.1000609 |
| Other Sources: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752191/pdf/ |
| Terms of Use: | This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA |
| Citable link to this page: | http://nrs.harvard.edu/urn-3:HUL.InstRepos:4882983 |
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