Our findings provide further evidence that in Taiwan, cigarette smoking may play the most harmful role in the initial development of gastric cancer, and that drinking alcohol may promote the process.

Mutations in hepatitis B virus (HBV) reverse transcriptase (RT) are associated with nucleos(t)ide analogue (NA) resistance during long-term antiviral treatment. However, the characterization of mutations in HBV RT in untreated patients has not yet been well illustrated. The objective of this study was to investigate the characterization and clinical significance of natural variability in HBV RT in treatment-naive patients. HBV RT sequences were analyzed in 427 patients by Sanger sequencing and in 66 patients by next-generation sequencing. Primary or secondary NA resistance (NAr) mutations were not found, except A181T in RT (rtA181T) by Sanger sequencing, but they were detected by next-generation sequencing. Mutations were found in 56 RT amino acid (aa) sites by Sanger sequencing, 36 of which had mutations that could lead to changes in B or T cell epitopes in the RT or S protein. The distribution of mutations was diverse in different sections within the RT region. Multiple mutations showed significant association with HBV DNA, HBsAg, HBeAg, age, and severity of liver fibrosis. Mutations at rt251, rt266, rt274, rt280, rt283, rt284, and rt286 were found most in the advanced liver disease (ALD) group by next-generation sequencing. The present study demonstrates that next-generation sequencing (NGS) was more suitable than Sanger sequencing to monitor NAr mutations at a low rate in the treatment-naive patients, and that mutations in the RT region might be involved in the progression to ALD.

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Our results revealed RIG-I enhanced IFN-α response by promoting antiviral protein expression via the STAT1 pathway. RIG-I may be a new predictive factor for prediction of IFN-α efficacy in CHB patients.