title: Interferon γ-induced protein 10 kinetics in treatment-naive versus treatment-experienced patients receiving interferon-free therapy for hepatitis C virus infection: implications for the innate immune response.
abstract: We measured interferon γ-induced protein 10 (IP-10) levels in 428 patients at baseline, week 1, and week 2 of all-oral treatment for hepatitis C virus (HCV) infection. An increased baseline IP-10 level was associated with a T allele in the IL28B gene, an increased alanine aminotransferase level in treatment-naive but not experienced patients, and an increased body mass index. At week 1, the mean decline in plasma IP-10 levels was the same in treatment-naive and treatment-experienced patients (-49%), whereas during week 2 the mean decline in IP-10 levels in treatment-naive patients (-14%) was significantly larger than in treatment-experienced patients (-2%; P = .0176). IP-10 thus may be a surrogate marker of the rate of intracellular viral replication complex decay.
authors.affiliation: University of California-San Diego, La Jolla.
authors.forename: Jennifer C
authors.initials: JC
authors.lastname: Lin
authors.affiliation: Pôle Hépato-digestif, Hôpitaux Universitaires de Strasbourg Inserm 1110 Université de Strasbourg, Strasbourg, France.
authors.forename: François
authors.initials: F
authors.lastname: Habersetzer
authors.affiliation: Fundacion de Investigacion de Diego, San Juan, Puerto Rico.
authors.forename: Maribel
authors.initials: M
authors.lastname: Rodriguez-Torres
authors.affiliation: Beth Israel Deaconess Medical Center, Boston, Massachusetts.
authors.forename: Nezam
authors.initials: N
authors.lastname: Afdhal
authors.affiliation: Alamo Medical Research, San Antonio, Texas.
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Lawitz
authors.affiliation: Gilead Sciences, Foster City, California.
authors.forename: Matthew S
authors.initials: MS
authors.lastname: Paulson
authors.affiliation: Gilead Sciences, Foster City, California.
authors.forename: Yanni
authors.initials: Y
authors.lastname: Zhu
authors.affiliation: Gilead Sciences, Foster City, California.
authors.forename: Gangadharan Mani
authors.initials: GM
authors.lastname: Subramanian
authors.affiliation: Gilead Sciences, Foster City, California.
authors.forename: John G
authors.initials: JG
authors.lastname: McHutchison
authors.affiliation: Johns Hopkins University School of Medicine, Baltimore, Maryland.
authors.forename: Mark
authors.initials: M
authors.lastname: Sulkowski
authors.affiliation: University of California-San Diego, La Jolla.
authors.forename: David L
authors.initials: DL
authors.lastname: Wyles
authors.affiliation: University of California-San Diego, La Jolla.
authors.forename: Robert T
authors.initials: RT
authors.lastname: Schooley
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D054357:Chemokine CXCL10 / Q000097:blood*; D005260:Female; D016174:Hepacivirus / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D008297:Male; D008875:Middle Aged; D010949:Plasma / Q000737:chemistry
chemical_list: D000998:Antiviral Agents; C114753:CXCL10 protein, human; D054357:Chemokine CXCL10
keywords: IP-10; direct-acting antiviral therapy; hepatitis C; innate immunity