Sofia Marques and Pedro SimasViral Pathogenesis Unit
Institute of Microbiology and Institute of Molecular Medicine
Faculty of Medicine
University of Lisbon
Author Summary
Persistent viruses present a major challenge to the immune response. Gamma-herpesviruses are a prime example, and the archetypal family member, Epstein-Barr virus, has been studied for many years. A major unanswered question with EBV is why long-term virus loads - a key pathogenesis outcome - vary so widely between individuals. As most EBV studies are necessarily descriptive, the murid gamma-herpesvirus, MuHV-4, provides an important focus of pathogenesis research. In this study (PLoS Pathogens 4(10): e1000177) we used MuHV-4 to address what determines long-term gamma-herpesvirus loads. We find a major role for a single MHC class I-restricted latency epitope. This reflects that latency-associated viral immune evasion and transcriptional silencing create a unique setting, in which the pool of possible epitopes is small enough to for epitope loss to have a significant impact on viral fitness. Our data suggest that polymorphisms in viral latency genes and in host HLA class I together, determine long-term viral loads.
Access to the article on the Internet is on:
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000177
Marques S, Alenquer M, Stevenson PG, and Simas JP (2008). A single CD8+ T cell epitope sets the long-term latent load of a Murid herpesvirus. PLoS Pathogens 4(10): e1000177.
