| First Author | McClellan KB | Year | 2006 |
| Journal | PLoS Pathog | Volume | 2 |
| Issue | 6 | Pages | e58 |
| PubMed ID | 16789842 | Mgi Jnum | J:162218 |
| Mgi Id | MGI:4818338 | Doi | 10.1371/journal.ppat.0020058 |
| Citation | McClellan KB, et al. (2006) Antibody-independent control of gamma-herpesvirus latency via B cell induction of anti-viral T cell responses. PLoS Pathog 2(6):e58 |
| abstractText | 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 gamma-herpesvirus 68 (gammaHV68) 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 gammaHV68 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 gamma-herpesvirus latency. Exploitation of this property of B cells may allow enhanced vaccine responses to chronic virus infection. |
