Long interspersed element-1 (LINE-1, L1) transposable element (TE) composes about 17% of the human genome. However, genetic and biochemical interactions between L1 and hepatitis B virus (HBV) remain poorly understood. In this study, I found that HBV restricts L1 retrotransposition in a reverse transcriptase (RT)-independent manner. Notably, HBV polymerase (Pol) strongly inhibited L1 retrotransposition. Indeed, the ribonuclease H (RNase H) domain was essential for inhibition of L1 retrotransposition. The L1 ORF1p RNA-binding protein predominantly localized into cytoplasmic RNA granule termed P-body. However, HBV Pol hijacked L1 ORF1p from P-body through an interaction with L1 ORF1p, when both proteins were co-expressed. Furthermore, HBV Pol repressed the L1 5' untranslated region (UTR). Altogether, HBV seems to restrict L1 mobility at multiple steps. Thus, these results suggest a novel function or activity of HBV Pol in regulation of L1 retrotransposition.