Premium
Upregulation of endogenous intrahepatic interferon stimulated genes during chronic hepatitis C virus infection
Author(s) -
MacQuillan Gerry C.,
Mamotte Cyril,
Reed William D.,
Jeffrey Gary P.,
Allan Jane E.
Publication year - 2003
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.10381
Subject(s) - isg15 , interferon , ribavirin , virology , hepatitis c virus , immunology , interferon stimulated gene , virus , viral quasispecies , gene , downregulation and upregulation , liver disease , genotype , alpha interferon , biology , medicine , effector , immune system , innate immune system , genetics , ubiquitin
The success of interferon‐α and ribavirin combination therapy for the treatment of chronic hepatitis C viral infection differs between patients. In an attempt to identify predictors of host response to therapy, the levels of mRNA for interferon (IFN) stimulated genes: MxA, PKR, 2′5′ OAS, ISG15, and interleukin 8 (IL‐8), were examined in liver by real‐time RT‐PCR prior to commencement of therapy. The levels of intrahepatic classical IFN stimulated genes, but not IL‐8, in chronic HCV disease (n = 44) were found to be significantly upregulated ( P < 0.001) compared to the control cohort (n = 12). The genotype of the infecting HCV strain did not influence IFN stimulated gene expression. These results suggest that the endogenous type 1 IFN antiviral effector pathway is broadly activated during chronic HCV disease, although the levels of mRNA for any of the IFN‐stimulated genes tested did not predict the outcome of combination therapy. J. Med. Virol. 70: 219–227, 2003. © 2003 Wiley‐Liss, Inc.