{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T02:40:32Z","timestamp":1791081632672,"version":"4.1.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":730,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Anti\u2013hepatitis B virus (HBV) nucleos(t)ides analogs (NA) exert selective pressures on polymerase (<jats:italic toggle=\"yes\">pol<\/jats:italic>) and surface (<jats:italic toggle=\"yes\">S<\/jats:italic>) genes, inducing treatment resistance and increasing the risk of vaccine escape mutants. The rate of emergence for these mutations is largely unknown in patients coinfected with human immunodeficiency virus (HIV) and HBV undergoing dual-active therapy. In a 3-year, repeat-sampling, prospective cohort study, HBV viral genome sequences of 171 HIV-HBV coinfected patients, presenting with HBV viremia for at least one visit, were analyzed every 12 months via DNA chip. Logistic and Cox proportional hazard models were used to determine risk factors specifically for <jats:italic toggle=\"yes\">S<\/jats:italic> gene mutations at baseline and during follow-up, respectively. HBV-DNA levels &gt;190 IU\/mL substantially decreased from 91.8% at inclusion to 40.3% at month 36 (<jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001), while lamivudine (LAM) or emtricitabine (FTC) use remained steady (71.9%) and tenofovir (TDF) use expanded (month 0, 17.5%; month 36, 66.7%; <jats:italic toggle=\"yes\">P<\/jats:italic> &lt; 0.001). The largest increase of any mutation class was observed in l-nucleoside\u2013associated <jats:italic toggle=\"yes\">pol<\/jats:italic> gene\/antiviral-associated <jats:italic toggle=\"yes\">S<\/jats:italic> gene mutations (cumulative incidence at the end of follow-up, 17.5%) followed by alkyl phosphonate-associated <jats:italic toggle=\"yes\">pol<\/jats:italic>-gene (7.4%), immune-associated <jats:italic toggle=\"yes\">S<\/jats:italic> gene (specifically any amino acid change at positions s120\/s145, 6.4%), and d-cyclopentane\u2013associated <jats:italic toggle=\"yes\">pol<\/jats:italic>-gene mutations (2.4%). Incidence of l-nucleoside\u2013associated <jats:italic toggle=\"yes\">pol<\/jats:italic>-gene\/antiviral\u2013associated <jats:italic toggle=\"yes\">S<\/jats:italic> gene mutations was significantly associated with concomitant LAM therapy (adjusted hazard ratio [HR], 4.61; 95% confidence interval [CI], 1.36-15.56), but inversely associated with TDF use (adjusted HR\/month, 0.94; 95% CI,0.89-0.98). Cumulative duration of TDF was significantly associated with a reduction in the occurrence of immune-associated <jats:italic toggle=\"yes\">S<\/jats:italic> gene mutations (HR\/month, 0.88; 95% CI, 0.79-0.98). No major liver-related complications (e.g., fulminant hepatitis, decompensated liver, and hepatocellular carcinoma) were observed in patients with incident mutations. <jats:italic toggle=\"yes\">Conclusion<\/jats:italic>: Vaccine escape mutants selected by NA exposure were frequent and steadily increasing during follow-up. Although the high antiviral potency of TDF can mitigate incident mutations, other antiviral options are limited in this respect. The public health implications of their transmission need to be addressed. 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