Associate Professor Peter Revill is a senior medical scientist and Head of Molecular Virology within the Division of Research and Molecular Development at VIDRL, Peter Doherty Institute for Infection and Immunity. He was appointed on contract in 2004, given tenure in 2007 and promoted to Section Head in 2011. He has over 25 year’s experience as a molecular virologist and is an internationally recognized expert on hepatitis B virus (HBV) pathogenesis, particularly the role of HBV splicing and HBV variants in disease progression and treatment response. He has had a very productive research career with over 60 publications, and has been lead or senior author on numerous publications in highly respected journals, including GUT, Nature Reviews Gastroenterology and Hepatology, Hepatology, The Journal of Hepatology and The Journal of Virology.
A/Prof Revill has a strong national and international reputation in HBV virology and pathogenesis. In 2015, with Professor Stephen Locarnini and Professor Fabien Zoulim, he initiated global HBV cure initiative, the “International Coalition to Eliminate HBV” (ICE-HBV), with a Perspectives paper published in “Nature Reviews Gastroenterology and Hepatology”. He has since been elected Chair of the ICE-HBV Governing Board (http://ice-hbv.org/). A/Prof Revill has contributed significantly to our understanding of HBV pathogenesis, particularly the role of genotypes and HBV variants, in disease pathogenesis, HIV-HBV co-infection, and regulation of innate immune responses. Most recently he led the team which showed BCP variants were associated with reduced likelihood of functional cure in the setting of antiviral therapy (Bayliss et al, GUT, 2016), with a follow up invited commentary also published in GUT (in press). He also led the team which showed that spliced HBV variants in serum are predictive of liver cancer (Bayliss J. Hepatol. 2013), following up from his earlier studies published in Hepatology (Preiss et al., 2008). He was also the first to show that the hepatitis B e antigen suppresses IL-18 signaling pathways, including production of the antiviral cytokine IFN-gamma (Jegaskanda J. Virol. 2014).