Downregulation of autophagy by herpesvirus Bcl-2 homologs.
The critical role of the cellular autophagy pathway in viral infection and pathogenesis has become increasingly apparent. Mounting evidences suggest that viruses have developed different strategies to meticulously modulate intracellular autophagy for their own benefits, thereby either promoting efficient viral replication or facilitating viral persistence. While our understanding of these strategies is still in its incipient stage, recent advances demonstrate that gamma herpesvirus Bcl-2 homolog (vBcl-2), which protects virus-infected cells from apoptosis, also suppresses cellular autophagy pathway through its direct interaction with the autophagy protein Beclin1. Interestingly, vBcl-2 has evolved to harbor the enhanced anti-autophagic activity compared to its host counterpart, suggesting an important role of cellular autophagy in response to viral infection and virus-associated pathogenesis. Thus, a detailed study of vBcl-2-mediated regulation of autophagy signal transduction pathway may lead to a better understanding of not only how virus escapes from host innate immunity but also how autophagy regulates viral infection and environmental stresses.
Liang
Chengyu
C
Department of Microbiology and Molecular Genetics and Tumor Virology Division, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772-9102, USA. chengyu_liang@hms.harvard.edu
E
Xiaofei
X
Jung
Jae U
JU
D000818:Animals; D001343:Autophagy / Q000502:physiology*; D015536:Down-Regulation; D018142:Gammaherpesvirinae / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D015398:Signal Transduction; D014764:Viral Proteins / Q000502:physiology*
D019253:Proto-Oncogene Proteins c-bcl-2; D014764:Viral Proteins