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Influence of the genetic heterogeneity of the ISDR and PePHD regions of hepatitis C virus on the response to interferon therapy in chronic hepatitis C
Author(s) -
PuigBasagoiti Francesc,
Sáiz JuanCarlos,
Forns Xavier,
Ampurdanès Sergi,
GiménezBarcons Mireia,
Franco Sandra,
SánchezFueyo Alberto,
Costa Josep,
SánchezTapias JoséMaría,
Rodés Juan
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.1098
Subject(s) - ns5a , interferon , virology , protein kinase r , hepatitis c virus , biology , virus , hepacivirus , interferon alfa , alpha interferon , protein kinase a , kinase , genetics , mitogen activated protein kinase kinase
Two genomic regions of hepatitis C virus (HCV), the interferon sensitivity‐determining region (ISDR) of the non‐structural 5A gene (NS5A) and the protein kinase‐RNA activated (PKR)‐eukariotic transcription factor (eIF2‐α) phosphorylation homology domain (PePHD) of the structural E2 gene, interact in vitro with the interferon‐inducible cellular PKR protein kinase. Mutations within these regions might, therefore, influence the response to interferon therapy. Viral load at baseline and sequence heterogeneity of HCV in NS5A and E2 regions was studied in 74 HCV‐1b and in 12 HCV‐3a infected patients with chronic hepatitis C who were treated with interferon. As previously reported by us, in a smaller series of patients in which the ISDR region was analyzed [Saiz et al. (1998) Journal Infectious Diseases 177:839–847], in the present study a low viral load and a high number of amino acid mutations within the ISDR, but not within the PePHD region, were significantly associated with long‐term response to interferon among HCV‐1b infected patients. No relationship between these viral features and response to therapy was disclosed in patients infected with HCV‐3a. J. Med. Virol. 65:35–44, 2001. © 2001 Wiley‐Liss, Inc.