Dr Helen Farrell

Biography

After completing my PhD under the mentorship of Prof Geoff Shellam at the University of Western Australia (UWA) in 1989, I spent 4 years at the University of Cambridge (UK) on a Royal Society Florey Fellowship in the molecular herpesvirus laboratory of Dr Tony Minson. I returned to UWA in 1994 where I initiated a research group investigating immune evasion strategies of cytomegalovirus, which was supported by NHMRC Priming and Project Grants. In 1998 I joined the Animal Health Trust (UK) where I continued these studies (part-time) supported by the BBSRC and The Wellcome Trust. In 2006, I came to Brisbane where I established a herpesvirus molecular pathology laboratory with Assoc Prof Nick Davis-Poynter at the UQ Clinical Medical Virology Centre (CMVC/SASVRC) on the Herston campus. These studies have been supported by NHMRC Project and NIH grants. In 2014, I joined Dr Philip Stevenson’s group and moved to SCMB in 2015 where I continue to work with animal models of herpesvirus infection, principally mouse cytomegalovirus.

Research Interest

My research interests have focused on the role of G protein-coupled receptor (GPCR) homologues of CMV that have a major impact on the ability of the virus to disseminate in the host and persist in the salivary glands, which is a principle site of CMV transmission to naïve recipients. We use mouse CMV as the animal model to study the function of these viral GPCR using virus mutants to quantify phenotypic effects and transgenic mice to trace virus infection in particular cell types. Current projects include the evaluating the contribution of G protein-coupled signaling and constitutive endocytosis in the CMV GPCR phenotype (in collaboration with Prof Mette Rosenkilde, University of Copenhagen) and the role of the CMV GPCR in the establishment and reactivation of latent CMV infections (Rhonda Cardin, Cincinnati Children’s Medical Center, Ohio). As a member of Philip Stevenson’s laboratory, my research area is focused on mechanisms of CMV transmission, entry and spread to sites of persistence. The role of the host innate immune response in limiting CMV dissemination is also a subject of investigation.