Multicenter trial on mother-to-infant transmission of GBV-C virus
Evidence indicates that the GBV‐C or hepatitis G virus can cause persistent infection in humans, but little is known on the importance of vertical transmission. To assess the risk of mother‐to‐infant transmission and the clinical outcome of infected babies, we investigated 175 anti‐HCV positive moth...
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Veröffentlicht in: | Journal of medical virology 1998-02, Vol.54 (2), p.107-112 |
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Zusammenfassung: | Evidence indicates that the GBV‐C or hepatitis G virus can cause persistent infection in humans, but little is known on the importance of vertical transmission. To assess the risk of mother‐to‐infant transmission and the clinical outcome of infected babies, we investigated 175 anti‐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 transmission 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 use, HIV coinfection, HCV‐RNA positivity, and type of feeding were not correlated with GBV‐C transmission. GBV‐C RNA remained persistently positive in all infected babies but one baby who seroconverted to anti‐E2. Seven (35%) babies with GBV‐C alone developed marginally elevated ALT; the baby with HCV and GBV‐C co‐infection had the highest ALT peak value (664 IU/l). Seven of the 141 (5%) babies born to the GBV‐C RNA negative mothers acquired HCV and six (85.7%) had abnormal ALT. The mean 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 HCV became icteric. GBV‐C is frequently present in anti‐HCV positive women. The infection is transmitted efficiently from mother to baby and rate of transmission is much higher than that for HCV. GBV‐C can cause persistent infection in babies but usually without clear evidence of liver disease. J. Med. Virol. 54: 107–112, 1998. © 1998 Wiley‐Liss,Inc. |
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ISSN: | 0146-6615 1096-9071 |
DOI: | 10.1002/(SICI)1096-9071(199802)54:2<107::AID-JMV7>3.0.CO;2-A |