21). HBV/HCV dual-infected patients most often presented

with evidence of dual infection at baseline (88%), as determined by either dual positivity of HBV DNA and HCV RNA and/or serologic findings of HBsAg and anti-HCV. The remaining 12% were found to have become dual-infected with the second virus at least 3 months after the initial diagnosis of the first viral infection during the course of follow-up (8% had HBV before HCV, and 4% had HCV before HBV). The HCV genotype distribution was as follows: GSK-3 phosphorylation 55% genotype 1, 20% genotype 2 or 3, 25% genotypes 4-6 (n = 51). Monoinfected patients were significantly more likely to receive anti-HBV therapy during the course of their follow-up than patients with HBV and HCV dual infection (43% versus 24%; P = 0.002). Among those who received HBV antiviral therapy, the average duration of treatment was similar between the two study groups (38 ± 24 months versus 40 ± 29 months; P = 0.77). Dual-infected patients received anti-HCV therapy 28% of the time for

9 ± 3 months. Laboratory measurements evaluated at presentation including several markers of overall liver function were similar: alpha-fetoprotein, albumin, alkaline phosphatase, Ridaforolimus solubility dmso international normalized ratio for prothrombin time, total bilirubin, and HBV DNA and remained similar during the course of follow-up. These results are summarized in Table 2. At presentation, HBV/HCV dual-infected patients were categorized as negative for both viruses (dual-negative viral load results) or having an HBV-dominant infection (HBV DNA level greater than HCV RNA) or HCV-dominant infection (HCV RNA level greater than HBV DNA). Among dual-infected Asian patients, 14% presented with a negative viral load results for both viruses, Amylase whereas 25% of non-Asian patients presented with no detectable HBV or HCV (P = 0.21) (Table 3). HBV-dominant disease was

found in 38% of Asian patients and 10% of non-Asian patients (P = 0.02). Of the 38% of Asians with HBV-dominant infection, 83% had complete dominance (defined as negative HCV RNA with detectable HBV DNA), and 17% had partial HBV dominance (detectable HBV and HCV viral loads, but with HBV DNA level being greater than HCV RNA). All of the non-Asian patients with HBV-dominant disease displayed complete HBV dominance. Infection characterized by HCV dominance was found in 48% of Asian patients and 65% of non-Asian patients (P = 0.18). In this category, 70% of Asian patients had undetectable HBV DNA coupled with a positive HCV RNA, and 30% had detectable viral loads for both viruses. Similar results were found in non-Asian patients, with 62% of those with HCV-dominant disease having undetectable HBV DNA and 38% having detectable viral loads for both HBV and HCV.