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The efficacy and safety of maternal tenofovir disoproxil fumarate (TDF) in reducing mother-to-infant hepatitis B virus (HBV) transmissions is not clearly understood. We conducted a prospective, multicenter trial and enrolled 118 hepatitis B surface antigen (HBsAg)-and hepatitis B e antigen-positive pregnant women with HBV DNA 7.5 log 10 IU/mL. The mothers received no medication (control group, n 5 56, HBV DNA 8.22 6 0.39 log 10 IU/mL) or TDF 300 mg daily (TDF group, n 5 62, HBV DNA 8.18 6 0.47 log 10 IU/mL) from 30-32 weeks of gestation until 1 month postpartum. Primary outcome was infant HBsAg at 6 months old. At delivery, the TDF group had lower maternal HBV DNA levels (4.29 6 0.93 versus 8.10 6 0.56 log 10 IU/mL, P < 0.0001). Of the 121/123 newborns, the TDF group had lower rates of HBV DNA positivity at birth (6.15% versus 31.48%, P 5 0.0003) and HBsAg positivity at 6 months old (1.54% versus 10.71%, P 5 0.0481). Multivariate analysis revealed that the TDF group had lower risk (odds ratio 5 0.10, P 5 0.0434) and amniocentesis was associated with higher risk (odds ratio 6.82, P 5 0.0220) of infant HBsAg positivity. The TDF group had less incidence of maternal alanine aminotransferase (ALT) levels above two times the upper limit of normal for 3 months (3.23% versus 14.29%, P 5 0.0455), a lesser extent of postpartum elevations of ALT (P 5 0.007), and a lower rate of ALT over five times the upper limit of normal (1.64% versus 14.29%, P 5 0.0135) at 2 months postpartum. Maternal creatinine and creatinine kinase levels, rates of congenital anomaly, premature birth, and growth parameters in infants were comparable in both groups. At 12 months, one TDF-group child newly developed HBsAg positivity, presumably due to postnatal infection and inefficient humoral responses to vaccines. Conclusions: Treatment with TDF for highly viremic mothers decreased infant HBV DNA at birth and infant HBsAg positivity at 6 months and ameliorated maternal ALT elevations. (HEPATOLOGY 2015;62:375-386) D espite the 75%-90% reduction of chronic hepatitis B viral (HBV) infection following universal infant immunization, active/passive immunoprophylaxis has not eradicated mother-toinfant HBV transmission. [1][2][3][4] Approximately 10% of chronic HBV infections cannot be prevented.5-7 The major risks of chronic HBV infection in the immunization era are maternal hepatitis B surface antigen (HBsAg)/hepatitis B e antigen (HBeAg) positivity and high maternal viral load.5-9 Moreover, after immunoprophylaxis, children with HBV infection have a higher risk of developing hepatocellular carcinoma. 10,11 To achieve the goal of global eradication of HBV infection, better strategies aimed at interrupting Abbreviations: ALT, alanine aminotransferase; anti-HBs, antibody to hepatitis B surface antigen; D0, day 0, initiation of TDF treatment (baseline); D1M, 1 month after TDF treatment; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HBV, hepatitis B virus; P0, at partum; PXM, X months postpartum; SNR, signal-to-noise ratio; TDF, tenofov...

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Mutants ofHepatitis B virus (HBV) infection is a global health problem and is the major cause of hepatitis, liver cirrhosis, and hepatocellular carcinoma. 1 Hepatitis B virus surface antigen (HBsAg) contains the dominant neutralizing epitopes of HBV and is thus used in current vaccines. Nine different subtypes of HBsAg have been identified, and each consists of a common group-specific (a) determinant and 2 sets of subtype-specific (d/y, w/r) determinants. 2