Management of chronic hepatitis B in pregnancy

Pregnancy associated with chronic hepatitis B (CHB) is a common and important problem with unique challenges. Pregnant women infected with CHB are different from the general population, and their special problems need to be considered: such as the effect of hepatitis B virus (HBV) infection on the mother and fetus, the effect of pregnancy on replication of the HBV, whether mothers should take HBV antiviral therapy during pregnancy, the effect of these treatments on the mother and fetus, how to carry out immunization of neonates, whether it can induce hepatitis activity after delivery and other serious issues. At present, there are about 350 million individuals with HBV infection worldwide, of which 50% were infected during the perinatal or neonatal period, especially in HBV-endemic countries. Currently, the rate of HBV infection in thechild-bearing age group is still at a high level, and the infection rate is as high as 8.16%. Effective prevention of mother-to-child transmission is an important means of reducing the global burden of chronic HBV infection. Even after adopting the combined immunization measures, there are still 5%-10% of babies born with HBV infection in hepatitis B e antigen positive pregnant women. As HBV perinatal transmission is the main cause of chronic HBV infection, we must consider how to prevent this transmission to reduce the burden of HBV infection. In this population of chronic HBV infected women of childbearing age, specific detection, intervention and follow-up measures are particularly worthy of attention and discussion.

Specific anti-viral effects of RNA interference on replication and expression of hepatitis B virus in mice

Background RNA interference （RNAi） is a powerful tool to silence gene expression post-transcriptionally. Our previous study has demonstrated that small interfering RNAs （siRNAs） have sufficiently inhibited hepatitis B virus （HBV） replication and expression in vitro. In this study we observed the RNAi-mediated inhibitory effects on HBV replication in mice models and accessed the specificity of these effects. Methods A mutant RNAi vector （pSI-C mut） with two base pairs different from the original target gene sequence at the RNAi vector （pSI-C） was constructed according to the method described in this study, A mouse model of acute hepatitis B virus infection was established by injecting naked plasmid pHBV1.3 via the tail vein with acute circulatory overload, pSI-C, pSI-C mut and the irrelevant RNAi control plasmid for green fluorescent protein （GFP） gene, pSIGFP were respectively delivered with pHBV1.3 by tail vein injection method. Six days post injection, enzyme-linked immunosorbent assay （ELISA） assay was used to measure the concentration of HBV surface antigen （HBsAg） in mouse serum, immunohistochemical straining method was used to visualize the expressin of HBV core protein （HBcAg） in liver tissues, and the transcriptional level of HBV C mRNA in liver tissues was detectedd by reverse transcriptase PCR （RT-PCR） analysis. Results Injection of pSI-C exerted magnificent and specific inhibitory effects on the replication and expression of HBV in the murine model. After 6-day post-injection （ p. i. ）, the OD values were shown to be 5.07 ± 1.07 in infecting group and 0.62 ± 0. 59 in pSI-C group. The concentration of HBsAg in pSI-C group was significantly lower than that in infecting group （ P 〈 0. 01 ）. Liver intracellular synthesis of viral core protein was sharply reduced to 0. 9% ±0. 1%, compared with 5.4% ± 1.2% of positive hepatocytes in infecting group （P 〈0. 01 ）, and the transcriptional level of HBV C mRNA was greatly reduced by 84. 7%. However, the irrelevant RNAi control plasmid （pSIGFP）, and the pSI-C mut did not show the same robust inhibitory effects as pSI-C. Conclusion pSI-C exert efficient and specific inhibitory effects on HBV replication and expression in mice models.