Mother-to-infant transmission of Hepatitis C Virus (HCV), although uncommon (about 5% of infected pregnancies), represents the major cause of pediatric HCV infection. In the present work we wanted to investigate the role of HLA-G and C molecules in fetal infection. Among 357 pregnancies of HCV-RNA+ mothers, 20 infants (11 females and 9 males) were infected, i.e. steadily positive for HCV-antibody and HCV-RNA over 20 months of age. As a control group we randomly enrolled 43 uninfected babies, born to HCV-RNA+ mothers, but steadily negative for HCV-RNA during a follow-up of 2 years. All subjects (54 mothers and 63 children) underwent genomic typing for HLA-C polymorphism using the PCR-SSP technique. PCR-RFLP technique was used for HLA-G typing. The following HLA-G alleles were found: HLA-G*01011, 01012, 01013 and 0105N. HLA-G*01012 was more frequent in HCV positive babies (55%) than in negative ones (40.2%), than in mothers (36.6%) and in blood donors (35.8%). HLA-G*01012 was particularly present in infected males (66.6%). On the contrary, HLA-G*01011 was more represented in HCV negative babies (49% vs 40%). The null allele G*0105N was more frequent among HCV positive mothers than in controls (4.45% vs 1.85%) but it was equally highly distributed among the children (5% in positive and 4.6% in negative ones). HLA-Cw*07 frequency was 35% in HCV positive babies and 19.8% in HCV negative babies, 23% in mothers and 24% in blood donors. HLA-C alleles were divided in two groups according to the dimorphism at 77 and 80 amino acid residues: SN vs NK. The SN/NK. heterozygous genotype was prevalent among HCV uninfected babies (44.19% vs 25%) while SN homozygous genotype was more frequent in HCV+ babies (50% vs 32%). No linkage disequilibrium was observed between HLA-C and HLA-G alleles in this sample so their contribute might be independent.
|Number of pages||1|
|Journal||European Journal of Immunogenetics|
|Publication status||Published - 2001|
ASJC Scopus subject areas