An estimated 240 million people worldwide are chronically infected with hepatitis B virus (HBV). Chronic HBV infections often lead to the development hepatocellular carcinoma (HCC) and liver cirrhosis. Currently, there is a prophylactic vaccine that many of us receive in order to prevent infection and chronic disease; however, HBV has remained a serious health concern in some areas of the world. Moreover, there is no cure for chronic HBV infection.

Recent studies regarding the mechanism of entry for HBV infection have shed light on new therapeutic targets, such as the sodium taurocholate co-transporting polypeptide (NTCP), which is required for viral infection. My research aims to further elucidate the mechanisms by which viral entry and infection occur and more specifically the mechanism of fusion. To date, there is very little understood regarding the entry mechanism of HBV. Previous studies have shown that there is a likely fusion peptide at the N-terminus of the small surface protein, which is required for viral entry. Additionally, a portion of the large surface protein may play a role in fusion as well as a putative cholesterol recognition/interaction amino acid consensus (CRAC) domain, which may help stabilize binding of the HBV surface proteins to the host cell receptors.

Using a combination of structural studies and molecular biology approaches, I hope to gain new insight into the structural rearrangements and virion and host cell requirements that contribute to the fusion process.