S gene mutations of HBV in children with HBV-associated glomerulonephritis

Total 53 subjects, including 30 HBV-GN, 5 nephrosis with HBV carriers (control group 1), and 18 HBV carriers (control group 2) were included in this study. Polymerase chain reaction (PCR) was used to detect the HBV-GN S gene mutation.(1) The serotype of HBV was adw in the majority (52/53) of subjects, and was adr in only 1 subject in the control group 2; (2) the genotype of HBV was the type B in 51 subjects, the type E in 1 HBV-GN child, and the type C in 1 HBV carrier; (3) Seventeen point mutations in the S gene of HBV were identified in 21 of 30 (70%) HBV-GN patients. Among them, 16 of 21 (76.2%) mutations may cause amino acid substitutions of the HBV proteins, which occur predominantly (11/16 mutations) at threonine, serine or tyrosine phosphorylation sites of mitogen-activated protein kinase (MAPK) or protein tyrosine kinase (PTK). (4) In addition, single nucleotide mutations without amino acid substitutions (same sense mutation) were found in 2 subjects in each control group and 5 subjects in HBV-GN group.HBV S gene mutations and the subsequent amino acid substitutions in HBV proteins were found in most children with HBV-GN, suggesting that these mutations may play an important role in the pathogenesis of HBV-GN.Hepatitis B viruses (HBV) are well-recognized as the causes of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. In addition, HBV infection is also associated with a spectrum of extrahepatic manifestations [1]. Hepatitis B is prevalent in China and hepatitis B virus-associated glomerulonephritis (HBV-GN) is one of the common renal damages secondary to HBV infection in Chinese children [2]. The mechanism of HBV-GN is generally believed to be related to HBV-related immune reactions [3]. This is based on the findings that HBV viral antigens were detected in kidney tissue [4,5], and further HBV surface antigen (HBsAg) and HBV nucleus antigen were detected in the glomerular deposits [6]. However, the precise pathogenesis of HBV-GN is not fully unde