Pathogenesis of murine gammaherpesvirus 68 infection
Herpesviruses cause a wide range of diseases in humans and animals. A major programme in the lab investigates the mechanisms of pathogenesis in murine gammaherpesvirus 68 (MHV-68) infections. MHV-68 is a virus of small rodents which provides an important model system for studying gammaherpesviruses pathogenesis. MHV-68, like other herpesviruses, encodes a number of genes which interact with the host immune system to enable the virus to replicate and establish latent infection. Our lab uses virus mutants to study the role of individual gene products in virus pathogenesis and molecular and biochemical approaches to elucidate their function. We are particularly interested in the role of the innate immune system in control of infection eg the role of interferons, macrophages and NK cells.
MHV-68 infection can result in fibrotic disease and provides a model for studying the development and resolution of fibrosis. We have shown that in the absence of IFN-gamma, alternative activation of macrophages results in transient fibrosis which is associated with control of virus latent infection. We have a particular interest in virus encoded immunomodulatory molecules and have recently identified a novel chemokine binding molecule which binds a range of chemokines thereby down regulating the host immune response.