The transmission of hepatitis B virus (HBV) infection from mother-to-infant (MTI) and the susceptibility of offspring to hepatitis B under intrauterine exposure to HBsAg.

Abstract

Hepatitis B virus (HBV) causes long-term injury to the liver in patients with chronic hepatitis B. It was reported that nearly half of this disease's cases now result from mother-to-infant (MTI) transmission. Therefore, intervention during this period of transmission of HBV could effectively prevent HBV infection in infants. This study employed bioinformatics methods to analyze the datasets of MTI hepatitis B transmission obtained from the Gene Expression Omnibus (GEO) database. Through this analysis, we extracted valuable information to identify genes exhibiting differential expression and uncover the associated signal pathways. Ultimately, our investigations into alterations in immune function shed light on the underlying mechanisms of MTI HBV transmission. There were 593 genes that were significantly differentially expressed (512 up-regulated genes and 81 down-regulated genes) in the offspring CD8+T cells with Hepatitis B surface antigen (HBsAg) intrauterine exposure. The pathways enriched for differentially expressed genes have been revealed. Furthermore, we performed a correlation analysis between differentially expressed genes and maternal hepatitis B inheritance via the weighted gene co-expression network analysis (WGCNA) and eventually found a high correlation between the cyan module and the shape. Among them, there were 166 genes in the cyan module, which were mainly enriched in the phosphatidylinositol signaling system, glycerolipid metabolism, and other types of O-Glycan biosynthesis. Therefore, we speculated that these signaling pathways and the genes within may be closely related to hepatitis B susceptibility and maternal hepatitis B inheritance. In this study, we showed that differentially expressed genes and signaling pathways may be valuable in preventing MTI transmission of HBV.