A unique feature of hepatitis B virus (HBV) infection in humans is that viral clearance heavily depends on the age of exposure. However, the reason for this remains unclear. To understand the mechanism(s) of age-dependent outcomes of HBV infection in humans, we established an age-related HBV mouse model in which 3-week-old (B3C) BALB/c exhibited virus tolerance, while 6-week-old (B6C) counterparts represented virus clearance. Sterilization of gut microbiota from 3 to 6 wk of BALB/c using antibiotics prevented B6C mice from rapidly clearing HBV. To further delineate the effect of gut bacteria, antibiotic (ABX)-treated BALB/c mice were either cohoused with the undisturbed counterparts (cohouse group) or recovered alone (self-recovery group) from 6 to 10 weeks of age. The 3 groups of BALB/c mice, i.e., control, cohousing, and self-recovery, were administered HDI at 10 weeks of age. While the former two groups cleared HBsAg at 4 wpi, 50% of the mice in self-recovery group were still HbsAg positive at the same time, which is similar to that of in ABX treated B6C mice. Altogether, BLAB/c showed gut bacterial-dependent HBV clearance. To understand the influence of gut bacteria on liver liiunity, the dynamics of hepatic myeloid and lymphoid cell populations were investigated. Our results show that TNFα-secreting Ly6C+ monocytes were significantly reduce at D3 in ABX treated B6C mice. In addition, the expansion of CD8+ T-cell at D7 was not seen in this mouse group. These data collectively suggest that altered gut microbiota can shape liver immune responses to HBV which in turn result in viral clearance/persistence.