title: Interleukin 28B rs12979860 (CT/TT) genotype is associated with milder hepatic damage in the natural evolution of HCV/HIV coinfection.
abstract: Hepatitis C virus (HCV)/human immunodefficiency virus (HIV) coinfection is a major health problem, affecting mostly to individuals with exposure to blood products, as hemophiliacs or intravenous drug users, or those exposed to high-risk sexual practices. Genotyping of interleukin 28B (IL-28B) rs12979860 polymorphism is a useful tool for guiding therapeutic decisions in this disease. On the contrary, there is not enough information on the pathogenic role of this polymorphism in the natural history of the disease. The objective of this study is to describe the relationships between the CT/TT genotype of this polymorphism with viral loads and also with a number of biomarkers of liver function in coinfected patients naïve for treatment for HCV. Seventy-five HCV/HIV coinfected patients were retrospectively recruited in our Hospital from 2010 to 2011. Logistic regression analysis adjusting by [Age], [Sex], [HCV viral genotype], [HCV viral load], [HIV viral load], and [CD4 T cells levels] revealed the IL-28B rs12979860 (CT/TT) genotype as a protective factor against alanine aminotransferase (ALT) levels (>100 IU/L), aspartate aminotransferase (AST) levels (>75 IU/L), and AST-to-platelet ratio index (APRI) score for liver fibrosis (>1.5) [OR, (95% CI), p]: ALT [0.026 (0.001-0.576) 0.021]; AST [0.001 (0.000-0.297) 0.019]; APRI [0.031 (0.002-0.41) 0.008]. Stepwise regression analysis considering the same adjusting variables showed the same results. In consequence, the IL-28B rs12979860 (CT/TT) genotype, which is a marker of poor response to HCV treatment, could be mediating on the contrary a certain protective effect against the hepatic damage caused by this virus in patients coinfected by HIV.
authors.affiliation: Clinical Analysis Service, Hospital Clínico Universitario-SACYL, Valladolid, Spain.
authors.forename: Concha
authors.initials: C
authors.lastname: de la Fuente
authors.forename: Carmen
authors.initials: C
authors.lastname: Hinojosa
authors.forename: Isabel
authors.initials: I
authors.lastname: Gilabert
authors.forename: Maria Ángeles
authors.initials: MÁ
authors.lastname: Jiménez Sousa
authors.forename: Jose Manuel
authors.initials: JM
authors.lastname: González
authors.forename: Raúl
authors.initials: R
authors.lastname: Ortiz de Lejarazu
authors.forename: Ana
authors.initials: A
authors.lastname: Loma
authors.forename: Concepción
authors.initials: C
authors.lastname: Nieto
authors.forename: Rosa
authors.initials: R
authors.lastname: Arnaiz
authors.forename: Jesús F
authors.initials: JF
authors.lastname: Bermejo-Martin
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000378:metabolism; D023241:Antiretroviral Therapy, Highly Active; D001219:Aspartate Aminotransferases / Q000378:metabolism; D060085:Coinfection / Q000188:drug therapy / Q000235:genetics / Q000821:virology; D005838:Genotype; D006678:HIV / Q000187:drug effects / Q000235:genetics; D015658:HIV Infections / Q000188:drug therapy / Q000235:genetics* / Q000821:virology; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics; D006526:Hepatitis C / Q000188:drug therapy / Q000235:genetics* / Q000821:virology; D006801:Humans; D007372:Interferons; D007378:Interleukins / Q000235:genetics*; D016014:Linear Models; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D008875:Middle Aged; D015999:Multivariate Analysis; D020641:Polymorphism, Single Nucleotide; D012189:Retrospective Studies; D000095022:Interferon Lambda
chemical_list: D000410:Alanine Transaminase; D001219:Aspartate Aminotransferases; D007372:Interferons; D007378:Interleukins; C000624353:interferon-lambda, human; D000095022:Interferon Lambda