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Evolution of the E2 region of hepatitis C virus in an infant infected by mother‐to‐infant transmission
Author(s) -
Sitia Giovanni,
Cella Davide,
De Mitri Maria Stella,
Novati Roberto,
Foppa Caterina Uberti,
Perackis Katarina,
Bianchi Cesare,
Lazzarin Adriano,
Morsica Giulia
Publication year - 2001
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1074
Subject(s) - viral quasispecies , virology , biology , population , genetics , virus , single strand conformation polymorphism , flaviviridae , polymerase chain reaction , hepatitis c virus , medicine , environmental health , gene
Abstract To demonstrate vertical transmission of hepatitis C virus from an HCV infected woman and to assess the evolution of HCV quasispecies in the infant, the variable E2 region was analyzed in one mother‐infant pair at birth and in serial samples from the infected baby. Sequence analysis of the E2 region obtained by means of direct sequencing of PCR products of mother‐infant pair at birth, showed that the sequence of the dominant strain in the infant was related closely but not identical to that of her mother. The HCV population in mother‐infant pair at birth and in serial samples of the infant was analyzed by polymerase‐chain reaction‐mediated Single Strand Conformational Polymorphism analysis (SSCP), which can distinguish DNA fragments of the same size as different electrophoretic migration of single stranded DNA. Single Strand Polymorphism analysis revealed that the infant was infected with two mutant genomes whereas the mother had a unique variant. The prevalent strain detected in the baby was not dominant in the mother at delivery and the pattern of quasispecies in the infant at birth was not the same as her mother, suggesting that the infant acquired the infection in utero. Changes in the dominant strain and evolution of the pattern of quasispecies in the infant from the 10th month of age were possibly due to the immune selection of escape mutants. J. Med. Virol. 64:476–481, 2001. © 2001 Wiley‐Liss, Inc.