Hamster (Golden Syrian) Hepatocytes, Suspension

The Feasibility of Establishing a Hamster Model for HBV Infection: In Vitro Evidence

Chronic HBV infection remains incurable, with research hampered by lack of immunocompetent small animal models. Here, Zhang's team explored the golden Syrian hamster as a potential model, beginning with in vitro assessment of HBV replication in primary hamster hepatocytes (PHaHs) via adenoviral HBV (Ad-HBV) transduction.

Due to low PHaH transfection efficiency, they employed adenoviral delivery. In HepG2 controls, Ad-HBV dose-dependently induced HBV DNA replication and cccDNA formation (Fig. 1A). Remarkably, cccDNA was readily detected in PHaHs (Fig. 1B), appearing as a 3.2 kb band after heat treatment and EcoR I linearization (Fig. 1C, lanes 1-4). Authenticity was confirmed by ExoI/III exonuclease resistance, leaving undigested cccDNA and CM-rDNA (Fig. 1C, lane 5)-both methods effectively distinguishing cccDNA from other HBV DNA species. These results demonstrate that PHaHs support HBV cccDNA formation via intracellular recycling. They next assessed HBV promoter activity by luciferase assay, with HepG2 and 293T cells as positive and negative controls. PHaHs supported all four major HBV enhancers/promoters (EnII/Cp, S1p, S2p, EnI/Xp) at levels comparable to HepG2 (Fig. 1D). Notably, S2p showed non-liver-specific activity as previously reported, but was somewhat more active in PHaHs. These data indicate PHaHs possess essential hepatic transcription factors for HBV transcription.