Antibody-independent control of γ-herpesvirus latency via B cell induction of anti-viral T cell responses

Kelly B. McClellan, Shivaprakash Gangappa, Samuel H. Speck, Herbert W. Virgin IV

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)578-590
Number of pages13
JournalPLoS pathogens
Volume2
Issue number6
DOIs
StatePublished - Jan 1 2006

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