Mother-to-Infant Transmission of Hepatitis C Virus. Part 2
The aim of the present study was to identify preventable risk factors associated with HCV transmission and to provide a basis for the prevention of HCV infection in newborns. For this purpose, we retrospectively evaluated virological and clinical parameters (e.g., mode and course of delivery) within a large, well-defined cohort of HCV-infected pregnant women. Although vaginal delivery itself was not a risk factor for transmission in the present study, we found that perinatal infantile hypoxia and vaginal or perineal laceration that occurred during vaginal delivery significantly increased the risk for HCV transmission.
Patients and Methods
Study populationThe study population included HCV-infected women who were being studied at the Institute of Virology (University of Vienna, Vienna) and who gave birth between 1994 and 1999. HCV infection was identified in these women, before or during pregnancy, by serologic detection of HCV-specific antibodies by use of an ELISA and was confirmed by detection of HCV RNA in serum by use of a reverse-transcriptase polymerase chain reaction (RT-PCR). For the RT-PCR–positive women, HCV load was determined with a quantitative PCR. For the RT-PCR–negative women, the specificity of the antibodies detected by ELISA was confirmed by use of an immunoblot. Furthermore, available serum samples were tested for maternal HIV coinfection according to World Health Organization guidelines. For women without information on HCV load or HIV infection, data were completed by retrospective testing of available serum samples (clinical specimens were stored at −80°C)
The children of these mothers were considered to be HCV uninfected if an HCV-specific RT-PCR done ⩾1 month after birth or an HCV-specific antibody test done ⩾12 months after birth or both were negative. They were considered to be HCV infected if HCV RNA was detected in at least one of their blood samples (umbilical cord blood was not tested)
Children were considered to be HIV-1 uninfected if they were antibody negative on ⩾1 occasion or had at least 2 PCR-negative samples, with at least 1 test done after age 6 months. They were considered to be HIV-1 infected if HIV-1 RNA was detected in at least one of their blood samples. Children with inadequate HIV-1 laboratory data were classified as indeterminate Virological investigationAntibodies to HCV were determined in plasma by ELISA (Monolisa anti-HCV PLUS; Sanofi Diagnostics Pasteur), as recommended by the manufacturer. Before testing of serum samples by PCR, HCV-RNA was extracted with a QIAamp Viral RNA kit (Qiagen). HCV RNA positivity was determined by a qualitative RT-PCR (Amplicor HCV Detection kit [detection limit, 20–1000 copies/mL]; Roche Diagnostic Systems), and HCV load was measured using a quantitative RT-PCR (Amplicor Monitor HCV Assay; Roche Diagnostic Systems). All HCV-PCR–positive results were confirmed by testing a different aliquot of the original sample, and the sensitivity of each qualitative RT-PCR was demonstrated in routine testing by coextraction and codetection of a positive control with ∼1000 copies/mL. For PCR-negative samples, the specificity of ELISA-positive results was confirmed by a recombinant immunoblot (Riba HCV 3.0; Chiron)