Molecular evolution of HCV genotype 2c persistent infection following mother-to-infant transmission

Molecular evolution of HCV genotype 2c persistent infection following mother-to-infant transmission The molecular evolution of HCV 2c in a case of vertical transmission was studied by comparing the virus quasispecies in the sera from the mother and from the child in a two-year follow-up. The positivity of HCV-RNA since the delivery accounted for an in-utero infection. The Core-E1 genome region (nt 928-1225) was amplified by polymerase chain reaction (PCR) from serum samples collected at delivery and at 3, 9, 18 and 24 months after birth. The RIBA pattern was characterised by isolated anti-c22 positivity in the serum from mother and in sera from the child during the first 9 months. Additional presence of anti-c33 was observed afterwards. Genetic relatedness among isolates and with a mother minor variant serum (Mo1.13) was found (mean variability ranged between 0.79% and 1.20%). From phylogenetic analysis this variant was identified as the origin of one of the two main lineages that included all isolates from child sera at 9, 18 and 24 months. The variability analysis has shown that high viral heterogeneity is present in the child serum collected at birth (3.16%). In this phase the d n /d s index (1.26%) indicates the presence of strong selective pressures. The development of child specific immune response at 9 th month was concurrent with the disappearance of two mutants at positions 11 and 104 of E1.This rare case of inutero mother-to-infant transmission can be considered as a model to elucidate the HCV quasispecies diversification during the first stage of infection. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Molecular evolution of HCV genotype 2c persistent infection following mother-to-infant transmission

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Publisher
Springer-Verlag
Copyright
Copyright © 2000 by Springer-Verlag/Wien
Subject
Legacy
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s007050050688
Publisher site
See Article on Publisher Site

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