TEMPORAL PROFILE OF HEPATITIS-C VIRUS-ANTIBODY AND GENOME IN INFANTS BORN TO MOTHERS INFECTED WITH HEPATITIS-C VIRUS BUT WITHOUT HUMAN-IMMUNODEFICIENCY-VIRUS COINFECTION
Yh. Ni et al., TEMPORAL PROFILE OF HEPATITIS-C VIRUS-ANTIBODY AND GENOME IN INFANTS BORN TO MOTHERS INFECTED WITH HEPATITIS-C VIRUS BUT WITHOUT HUMAN-IMMUNODEFICIENCY-VIRUS COINFECTION, Journal of hepatology, 20(5), 1994, pp. 641-645
To investigate mother-to-infant transmission of hepatitis C virus, ser
ial follow-up of anti-HCV and hepatitis C virus RNA was undertaken in
11 infants born to hepatitis C virus-infected mothers who had been scr
eened from 11688 pregnant women. None of the hepatitis C virus-infecte
d mothers was infected by human immunodeficiency virus. Anti-HCV was c
hecked by the second-generation enzyme immunoassay kit, and hepatitis
C Virus RNA was examined by reverse transcriptase-nested polymerase ch
ain reaction. Hepatitis C virus RNA was found in more than two serum s
amples in two of these 11 infants; those two infants were regarded as
hepatitis C virus-infected. One of the two had hepatitis C virus RNA a
t the age of 1, 3, and 6 months, but not later. The course of hepatiti
s C virus RNA and anti-HCV in this baby may reflect fluctuating viral
replication in chronic infectious disease or viral clearance in acute
infection. The other infant had hepatitis C virus RNA detectable at th
e age of 3 months and at 15, 18 and 24 months. In the other nine non-h
epatitis C virus-infected infants, maternally acquired anti-HCV gradua
lly disappeared by the age of 6 months. The liver function profile fel
l, to the normal range in all the infants, including the two hepatitis
C virus-infected infants. This may indicate the subclinical nature of
hepatitis C virus infection in infancy. Seven fathers and four siblin
gs of these 11 infants were checked for anti-HCV and liver function te
sts; none had evidence of hepatitis C virus infection. These results s
how that the rate of mother-to-infant transmission of hepatitis C viru
s from mothers without human immunodeficiency virus coinfection is abo
ut 18% and that hepatitis C virus infection in these patients seemed t
o run a subclinical course. (C) Journal of Hepatology.