Evidence indicates that the GBV-C or hepatitis G virus can cause persi
stent infection in humans, but little is known on the importance of ve
rtical transmission. To assess the risk of mother-to-infant transmissi
on and the clinical outcome of infected babies, we investigated 175 an
ti-HCV positive mothers and followed-up their children for 3-33 months
. GBV-C RNA was detected by RT-PCR and anti-E2 antibody was assayed by
EIA. Thirty-four (19.4%) women were GBV-C RNA positive and transmissi
on occurred to 21 (61.8%) babies; 20 (95.2%) acquired GBV-C alone, and
one (4.8%) GBV-C and HCV. Maternal factors such as intravenous drug u
se, HIV coinfection, HCV-RNA positivity, and type of feeding were not
correlated with GBV-C transmission. GBV-C RNA remained persistently po
sitive in all infected babies but one baby who seroconverted to anti-E
2. Seven (35%) babies with GBV-C alone developed marginally elevated A
LT; the baby with HCV and GBV-C co-infection had the highest ALT peak
value (664 IU/I). Seven of the 141 (5%) babies born to the GBV-C RNA n
egative mothers acquired HCV and six (85.7%) had abnormal ALT. The mea
n ALT peak value was significantly higher (P<0.05) for babies with HCV
than for those with GBV-C. None of the children with GBV-C or with HC
V became icteric. GBV-C is frequently present in anti-HCV positive wom
en. The infection is transmitted efficiently from mother to baby and r
ate of transmission is much higher than that for HCV. GBV-C can cause
persistent infection in babies but usually without clear evidence of l
iver disease. (C) 1998 Wiley-Liss, Inc.