Chronic　hepatitis　B　virus　(HBV)　infection　is　regarded　as　one　of　the　most　serious　infectious　diseases　and　a　significant　global　public　health　concern.　Although　the　neonatal　vaccine　has　been　effective　in　impeding　the　transmission　of　HBV,　tens　of　millions　of　HBV　patients　are　still　vulnerable　to　liver　disease　and　even　hepatocellular　carcinoma　(HCC).　In　this　research,　we　demonstrated　that　HBV-encoded　circRNA,　designated　as　HBV-circRNA-5,　was　involved　in　the　tumorigenesis　of　HCC.　Overexpression　of　HBV-circRNA-5　promoted　HCC　cell　proliferation　and　metastasis　in　vitro　and　promoted　HCC　tumor　growth　in　vivo.　Mechanistically,　HBV-circRNA-5　bound　to　miR-9-3p　selectively　and　resulted　in　the　upregulation　of　YAP/TAZ　expression,　which　consequently　stimulated　the　proliferation　of　HCC.　Overall,　we　provide　new　insight　into　understanding　carcinogenesis　and　the　progression　of　HBV-mediated　HCC,　as　well　as　clarify　a　new　cellular　mechanism　by　which　HBV　promotes　HCC　progression　through　the　HBV-circRNA-5/miR-9-3p/Hippo　network.IMPORTANCEHBV-mediated　cirrhosis　is　considered　a　significant　predisposing　danger　among　HCC　individuals　despite　the　increasing　incidence　of　HCC　due　to　noninfectious　factors.　However,　it　is　still　unclear　what　molecular　mechanisms　underlie　the　emergence　of　HBV-mediated　HCC.　This　study　identifies　HBV-encoded　circular　RNA　HBV-circRNA-5　as　a　critical　driver　of　HCC　progression,　with　the　capacity　to　promote　HCC　formation　through　the　miR-9-3p/Hippo　pathway.　In　summary,　our　study　developed　novel　insights　into　understanding　the　molecular　mechanism　behind　HBV-related　HCC　development　and　proposed　a　potential　target　for　HCC　treatment.