title: IL-10 and TNF-alpha polymorphisms and the recovery from HCV infection.
abstract: Hepatitis C virus (HCV) infection becomes chronic in about 85% of infected individuals, whereas only 15% of infected people clear spontaneously the virus. It is conceivable that the host immunogenetic background influences the course of infection in term of recovery. Thus, in this study we have evaluated the effect of functionally relevant polymorphisms at tumor necrosis factor-alpha (TNF-alpha, i.e., 2 biallelic polymorphisms at nt -863 and nt-308 of the promoter) and interleukin-10 (IL-10) loci (i.e., 1 biallelic polymorphism at nt -1082 of the promoter), on the clearance of HCV infection. To this purpose, we compared 18 Sicilian patients who had spontaneously recovered from previous HCV infection with 42 Sicilian patients with current HCV infection and 135 Sicilian healthy patients. The results demonstrate a decreased frequency of the -863CC TNF-alpha promoter genotype (involved in high production of this pro-inflammatory cytokine) and an increased frequency of the -1082GG IL-10 promoter genotype (involved in high production of this anti-inflammatory cytokine) in patients recovered from HCV infection. The evaluation of combined TNF-alpha and IL-10 genotypes revealed a significant increase of the "anti-inflammatory genotype" (low-TNF/high-IL-10 producers) in resolved HCV infection group compared with patients with persistent HCV infection. On the whole, our findings suggest that a genetically determined control of the HCV-induced inflammatory response may play a role in the resolution of HCV infection.
authors.affiliation: Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo, Palermo, Italy.
authors.forename: Domenico
authors.initials: D
authors.lastname: Lio
authors.forename: Calogero
authors.initials: C
authors.lastname: Caruso
authors.forename: Rosa
authors.initials: R
authors.lastname: Di Stefano
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Colonna Romano
authors.forename: Donatella
authors.initials: D
authors.lastname: Ferraro
authors.forename: Letizia
authors.initials: L
authors.lastname: Scola
authors.forename: Antonio
authors.initials: A
authors.lastname: Crivello
authors.forename: Anna
authors.initials: A
authors.lastname: Licata
authors.forename: L Mario
authors.initials: LM
authors.lastname: Valenza
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Candore
authors.forename: Antonio
authors.initials: A
authors.lastname: Craxì
authors.forename: Piero L
authors.initials: PL
authors.lastname: Almasio
mesh_terms: D000328:Adult; D005260:Female; D005838:Genotype; D006526:Hepatitis C / Q000235:genetics* / Q000276:immunology; D019698:Hepatitis C, Chronic / Q000235:genetics* / Q000276:immunology; D006801:Humans; D007124:Immunoenzyme Techniques; D016753:Interleukin-10 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D020641:Polymorphism, Single Nucleotide; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics* / Q000378:metabolism
chemical_list: D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10