The primary focus in the laboratory is to understand how HIV promotes liver inflammation and fibrosis through interactions with both activated hepatic stellate cells (HSCs) and liver macrophages (Kupffer cells). We were the first to identify the presence of CXCR4, one of the HIV co-receptors, on HSCs in vitro and in vivo (Hong F, Hepatology, 2009). Subsequently, we demonstrated that HIV and its envelope protein infects and elicits pro-inflammatory and profibrogenic effects on HSCs through interaction with CXCR4 (Tuyama A, Hepatology, 2010; Hong F, PLoS ONE, 2012). In addition, we have found that HIV robustly infects Kupffer cells and elicits a number of pro-inflammatory and pro-fibrogenic effects. In addition, we are exploring whether intrahepatic macrophages are a reservoir for HIV in patients on anti-retroviral therapies. Our work relies heavily on the use of primary human liver cells derived from both non-HIV infected and HIV-infected patients undergoing liver resection or transplant and is complemented using relevant cell lines.

In addition, the lab is interested in understanding mechanisms of non-alcoholic fatty liver disease (NAFLD) in both HIV and non-HIV infected patients. Dr. Bansal is involved in a number of clinical trials and translational studies focused on anti-fibrotic therapies, new HCV therapies, and novel treatments for NAFLD.