Antibody-Independent Control of γ-Herpesvirus Latency via B Cell Induction of Anti-Viral T Cell Responses

PLoS Pathogens

Herbert W. Virgin IV¹  Kelly B McClellan¹  Samuel H Speck²  Shivaprakash Gangappa³ 

[1] Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri, United States of America;Division of Microbiology and Immunology, Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia, United States of America;Emory Transplant Center, Emory University School of Medicine, Atlanta, Georgia, United States of America

关键词: B cells;    T cells;    Viral persistence;    latency;    Cytotoxic T cells;    Antibodies;    Viral replication;    Enzyme-linked immunoassays;    Viral genome;   

DOI  :  10.1371/journal.ppat.0020058

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

B cells can use antibody-dependent mechanisms to control latent viral infections. It is unknown whether this represents the sole function of B cells during chronic viral infection. We report here that hen egg lysozyme (HEL)-specific B cells can contribute to the control of murine γ-herpesvirus 68 (γHV68) latency without producing anti-viral antibody. HEL-specific B cells normalized defects in T cell numbers and proliferation observed in B cell−/− mice during the early phase of γHV68 latency. HEL-specific B cells also reversed defects in CD8 and CD4 T cell cytokine production observed in B cell−/− mice, generating CD8 and CD4 T cells necessary for control of latency. Furthermore, HEL-specific B cells were able to present virally encoded antigen to CD8 T cells. Therefore, B cells have antibody independent functions, including antigen presentation, that are important for control of γ-herpesvirus latency. Exploitation of this property of B cells may allow enhanced vaccine responses to chronic virus infection.

【 授权许可】

CC BY