| First Author | Freeman ML | Year | 2012 |
| Journal | J Immunol | Volume | 188 |
| Issue | 3 | Pages | 1049-56 |
| PubMed ID | 22198955 | Mgi Jnum | J:180759 |
| Mgi Id | MGI:5307183 | Doi | 10.4049/jimmunol.1102621 |
| Citation | Freeman ML, et al. (2012) Importance of antibody in virus infection and vaccine-mediated protection by a latency-deficient recombinant murine gamma-herpesvirus-68. J Immunol 188(3):1049-56 |
| abstractText | The human gamma-herpesviruses EBV and Kaposi's sarcoma-associated herpesvirus establish lifelong latent infections, can reactivate in immunocompromised individuals, and are associated with the development of malignancies. Murine gamma-herpesvirus-68 (gammaHV68), a rodent pathogen related to EBV and Kaposi's sarcoma-associated herpesvirus, provides an important model to dissect mechanisms of immune control and investigate vaccine strategies. Infection of mice with gammaHV68 elicits robust antiviral immunity, and long-term protection from gammaHV68 reactivation requires both cellular and humoral immune responses. Vaccination of mice with AC-replication and transcription activator (RTA), a highly lytic latency-null recombinant gammaHV68, results in complete protection from wild-type gammaHV68 infection that lasts for at least 10 mo. In this report, we examine the immune correlates of AC-RTA-mediated protection and show that sterilizing immunity requires both T cells and Ab. Importantly, Ab was also critical for mitigating viral infection in the brain, and in the absence of Ab-mediated control, amplification of the AC-RTA virus in the brain resulted in fatality. Our results highlight important considerations in the development of vaccination strategies based on live-attenuated viruses. |
