[Evolution of hepatitis G in children with vertically transmitted HGV]

Background A new hepatitis-associated RNA virus, belonging to the Flaviviridae, has been recently discovered and called HGV (GBV-C). This virus has been shown to be transmitted parenterally. In this study we examined a group of children born to HCV infected women. Methods Between September 1994 and December 1998, we studied a cohort of 53 pregnant women, aged between 20 and 43 years. They were all HCV Ab and HCV RNA positive, with a diagnosis of chronic hepatitis. One patient was HbsAg positive and 4 patients (pts.) (7.5%) were HIV Ab positive. Anamnestic information revealed that: 28 pts. (52.8%) were IVDUs, 11 pts. (20.8%) had been haemotransfused and 14 pts. (26.4%) had no risk factors. We examined HGV RNA by RT nested PCR, using primers from the 5'UTR of HGV. Anti-HGV antibodies (anti-E2) were detected with an ELISA test using recombinant E2 protein. Ten of the 53 pregnant women (18.9%) were HGV RNA positive (32 other pts., 60.4%, were positive for anti-E2 antibodies). We monitored their children for 18-24 months (with clinicai and haematological controls), looking for HGV RNA, anti-E2 antibodies, HCV RNA and for ALT serum levels. Results Seven (70%) new-bom children proved HGV RNA positive at follow-up; all babies were HCV RNA negative at controls. Four of them were born vaginally; none of them was breast-fed. HGV RNA was first detectable at the 3rd month of life in 3 babies, and all babies were HGV RNA positive at the 6th month of life. Six babies (85.7%) remained positive during the observation period. One baby (14.3%) seroconverted at 10 months, developing anti E-2 antibodies and becoming HGV RNA negative. Four babies (57.1%) maintained normal ALT serum levels during the whole follow-up period, while 3 patients showed a low increase in ALT serum levels. The ALT values normalised at later controls. Conclusions HGV infection shows a very high (70%) rate of vertical transmission but a low and doubtful pathogenicity with asymptomatic evolution in babies. Patients who did not develop anti-E2 antibodies at the 12th month of life remained infected without persistent signs of hepatic failure.