1 Department of Molecular Biology, Princeton University, Lewis Thomas Laboratory, Washington Road, Princeton, NJ, 08544, United States of America.
To better understand the origins of hepatitis delta virus (HDV), Perez-Vargas et al. sought to characterize the capability of HDV in utilizing envelope glycoproteins from viruses other than hepatitis B virus (HBV) (1). To this end, the authors compared the efficiency of HDV assembly and release in the presence of HBV surface antigens (HBsAg), vesicular stomatitis virus (VSV) G protein, or hepatitis C virus (HCV) E1 and E2 glycoproteins. The HDV particles generated with these respective glycoproteins were infectious to cells displaying appropriate receptors in vitro. HDV incorporation of VSV-G or HCV-E1E2 was assisted by farnesylation of the large hepatitis delta antigen (HDAg-L), a mechanism also seen with HBsAg.