Objective:To disclose the effect of miR-340-5p on HBV replication and its regulatory mechanism, furthermore provide new strategies for biomarkers and therapeutic drugs after HBV infection.Methods:The miR-340-5p mimic (340-mimic) and inhibitor (340-inhibitor) and their corresponding negative controls were transfected into liver cancer cells HepG2.2.15. The changes of HBeAg and HBsAg levels in the supernatant were detected by ELISA. At the same time, the RNA and the encapsidated DNA were extracted in collected cells, and qRT-PCR was used to detect the levels of HBV total RNA and pgRNA and the changes in HBV DNA copy numbers; qRT-PCR and Western blotting were used to verify the mRNA and protein expression of STAT3; in addition, after co-transformation of miR-340-5p mimic (340-mimic) and pEF-flag-stat3, the replication of HBV was detected by Northern blotting, qPCR and ELISA.Results:When miR-340-5p is overexpressed, the levels of total RNA produced by HBV transcription and the reverse transcription template pgRNA decreased significantly to 45.89% and 61.46% of the control group ( P=0.001, P=0.003); the synthesis of encapsidated DNA and the secretion levels of HBeAg and HBsAg were inhibited by 72.46%, 18.27% and 14.42% respectively ( P<0. 001, P<0. 001, P=0.005), while interference with endogenous miR-340-5p increased 44.02%, 45.56%, 22.66%, 11.85%, and 14.04% respectively compared with the control group ( P=0. 009, P=0. 080, P=0. 011, P=0.013, P=0.027). In contrast, overexpression of signal transducer and activator of transcription (STAT) 3 on this basis can attenuate the inhibition of HBV replication by miR-340-5p. The data also shows that STAT3 promotes HBV replication. Further experimental result also showed that STAT3 could promote the replication of HBV. Conclusions:miR-340-5p can suppress the transcription and translation of STAT3 by targeting it, thereby inhibiting the replication of HBV.

Objective:To clarify the effect and related factors of antiviral therapy on the change of esophageal varices in patients with hepatitis B virus-related cirrhosis.Methods:Fifty-two cases with hepatitis B virus-related cirrhosis who underwent endoscopy before and after antiviral therapy were selected from prospective cohorts. Patients were divided into three groups: no, mild, and moderate-severe based on the degree of esophageal varices. The changes in the severity of esophageal varices in each group were compared after antiviral therapy. Clinical characteristics (platelet, liver and kidney function, liver stiffness, and virological response) of patients with different regressions were analyzed. Measurement data were analyzed by independent sample t-test, one-way ANOVA, Mann-Whitney U test and Kruskal-Wallis H test, and Chi-Square test was used for count data.Results:All patients received entecavir-based antiviral therapy. The median treatment time was 3.1 (2.5-4.4) years. The proportion of patients without esophageal varices increased from 30.8% to 51.9%, the proportion of mild esophageal varices decreased from 40.4% to 30.8%, and the proportion of patients with moderate-to-severe esophageal varices decreased from 28.8% to 17.3% ( χ2=14.067, P=0.001). A total of 40.4% of patients had esophageal varices regression, and 13.5% had esophageal varices progression. The progression rate was significantly higher in patients with moderate-severe esophageal varices than patients with mild and no esophageal varices ( χ2=28.126, P<0.001), and 60.0% of patients with moderate-severe esophageal varices still remained in moderate-severe state after antiviral treatment. Baseline platelet count and 5-year mean change rates were significantly lower in patients with progressive moderate-to-severe esophageal varices than in those without progression (+3.3% vs. +34.1%, Z=7.00, P=0.027). Conclusion:After effective antiviral treatment, 40.4% of patients with hepatitis B virus-related cirrhosis combined with esophageal varices has obtained esophageal varices regression, but those with moderate to severe esophageal varices still have a considerable risk of progression while receiving mono antiviral treatment only. Thrombocytopenia and without significant improving are the clinical signs of progression risk after receiving antiviral treatment.