viral bcl-2-mediated evasion of autophagy aids chronic infection of γherpesvirus 68的自噬慢性感染艾滋病病毒bcl-2-mediated逃税γherpesvirus 68.pdfVIP

Viral Bcl-2-Mediated Evasion of Autophagy Aids Chronic Infection of cHerpesvirus 68 1,2. 3. 4. 1,4 4 5 Xiaofei E , Seungmin Hwang , Soohwan Oh , Jong-Soo Lee , Joseph H. Jeong , Yousang Gwack , 2 3 1,4 1,4 Timothy F. Kowalik , Ren Sun , Jae U. Jung *, Chengyu Liang * 1 Department of Microbiology and Molecular Genetics and Tumor Virology Division, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts, United States of America, 2 Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America, 3 Department of Molecular Medical Pharmacology, University of California, Los Angeles, California, United States of America, 4 Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California, United States of America, 5 Department of Physiology, University of California, Los Angeles, California, United States of America Abstract c-herpesviruses (cHVs) 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 c-herpesvirus 68 (cHV68) 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 mut