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According to a recent global systemic review, in 2010 about 248 million persons in the general population worldwide were chronically infected with hepatitis B virus (HBV), with the highest HBsAg prevalence rates being in Africa (8.83 %) and the Western Pacific region (5.26 %) [1]. Universal HBV vaccination programs in newborns have led a remarkable decline in HBsAg prevalence among young age groups in many countries such as China [2], but the huge number of persons with chronic HBV infection, if left untreated, will still cause an enormous disease burden associated with cirrhosis and hepatocellular carcinoma (HCC) in the next decades [3]. Long-term prospective cohort studies have shown that the serum level of HBV DNA is a key driver for disease progression from CHB to cirrhosis and HCC [4]. A Korean retrospective cohort study demonstrated that compensated cirrhosis patients, even with low viral load, were still at increased risk for HCC [5]. Pivotal clinical trials and reallife studies have shown that nucleoside or nucleotide analogs (NAs) have excellent efficacy in suppressing HBV DNA and improving liver biochemical tests. Furthermore, long-term therapy with NAs, especially entecavir (ETV) or tenofovir disoproxil fumarate (TDF), improves fibrosis or even early stage of cirrhosis as well as necroinflammation [6, 7]. More importantly, NA therapy improves clinical outcomes such as liver function reserve as measured by Child-Pugh or MELD scores, implicating that NAs could not only prevent compensated cirrhosis from decompensation but also reverse from decompensation to compensation (so-called recompensation) [8]. Therefore, antiviral therapy with highly potent and low resistance NAs such as ETV and TDF is recommended by major international guidelines including those recently released by WHO [9]. However, whether NA therapy could reduce the risk of HCC development is still an issue for discussion. A widely cited double-blind, randomized, placebo-controlled trial reported by Liaw et al. demonstrated that, in patients with advanced fibrosis or early cirrhosis, treatment with lamivudine could reduce the HCC if cases found within the first year were excluded from both groups, but the emergence of drug resistance compromised the benefit [10]. Clinical cohort studies from other centers in Hong Kong and Taiwan also showed a consistent trend of reduced incidence of HCC in patients treated with NAs [11, 12]. Furthermore, a population-based study carried out in Taiwan suggested that, compared with the pre-antiviral era, the incidence and mortality of HCC in the general population were decreasing with the increasing coverage rate of antiviral therapy for HBV and HCV, as shown in databases of medical insurance [13]. In addition, authors from US and Canada have also reported that NA treatment reduced the incidence of HCC in patients with CHB [14, 15]. In this issue of Hepatology International, Watanabe and coworkers [16] report that, in a retrospective cohort of 249 patients with CHB, 5 years after starting ETV treatment, liver functional reserve improved (prothrombin activity increased from 85.9 ± 17.4 to 97.0 ± 16.9 %, p\ 0.001, & Jidong Jia jia_jd@ccmu.edu.cn

Oral antiviral therapy reduces the risk of hepatocellular carcinoma in persons with chronic hepatitis B infection: combining evidence and common sense