E. Palomba et al., High rate of maternal-infant transmission of hepatitis G virus in HIV-1 and hepatitis C virus-infected women, ACT PAEDIAT, 88(12), 1999, pp. 1392-1395
The prevalence of hepatitis G virus (HGV) infection was investigated in 56
mothers with both human immunodeficiency virus type 1 (HIV-I) and hepatitis
C virus (HCV) infection. Thirty-three (58.8%) women had markers of HGV inf
ection, including 7/15 (46.6%) with no history of parenteral exposure to bl
ood. Sixteen (48%) had HGV RNA in serum by a polymerase chain reaction assa
y and 17 (52%) had antibody to E2, viral protein. No woman was positive for
both markers. Of 20 infants born to the 16 mothers with HGV viremia, 9 (45
%, 95% CI 34-58%) acquired the infection. No infected child seroconverted t
o HGV during the first year of life. At the latest visit (mean: 37.1 mo, ra
nge: 9-89 mo)7 children were still seronegative HGV RNA carriers, was both
RNA- and antibody-negative, while 1 RNA-negative child had developed the E2
antibody. Of the 20 HGV-exposed infants, 2 contracted HCV and 1 HIV-I (all
3 with HGV coinfection). No abnormalities in clinical findings and ALT lev
els were observed throughout the follow-up period in the six children with
HGV infection alone. Our findings show that HGV infection is widespread amo
ng HIV-1- and HCV-infected women. Maternal-infant transmission of HGV is co
mmon and occurs independently from that of HIV-I and HCV in women with trip
le infection. Most perinatally HGV-infected children develop persistent inf
ection with no clinical or biological signs of liver damage, at least in th
e first years of life.