Abstract
BackgroundThe CCR5 receptor, expressed on Th1 cells, may influence clinical outcomes of HCV infection. We explored a possible link between a CCR5 32-base deletion (CCR5delta32), resulting in the expression of a non-functioning receptor, and clinical outcomes of HCV infection.Methods CCR5 and HCV-related phenotypes were analysed in 1,290 chronically infected patients and 160 patients with spontaneous clearance.ResultsCarriage of the CCR5delta32 allele was observed in 11% of spontaneous clearers compared to 17% of chronically infected patients (OR = 0.59, 95% CI interval 0.35–0.99, P = 0.047). Carriage of this allele also tended to be observed more frequently among patients with liver inflammation (19%) compared to those without inflammation (15%, OR = 1.38, 95% CI interval 0.99–1.95, P = 0.06). The CCR5delta32 was not associated with sustained virological response (P = 0.6), fibrosis stage (P = 0.8), or fibrosis progression rate (P = 0.4).ConclusionsThe CCR5delta32 allele appears to be associated with a decreased rate of spontaneous HCV eradication, but not with hepatitis progression or response to antiviral therapy.
Highlights
Hepatitis C virus (HCV) infects about 2.8% of the global population [1] and is a major cause of chronic liver disease and hepatic mortality worldwide [2,3]
Multiple host genetic polymorphisms affecting HCVrelated liver inflammation, fibrosis progression and response to therapy have been reported encompassing a broad variety of genes, including IFNL3, associated with spontaneous and treatment-induced HCV clearance [5,6,7,8,9], as well as several genes recently associated with accelerated fibrosis progression rate
Numbers are the proportion of patients with the indicated feature. 1Gender was missing in 1 patient with spontaneous clearance. 2Age at estimated date of infection for patients with chronic infection, at cohort entry for those with spontaneous clearance. 3HCV genotype was missing in most patients with spontaneous clearance and in 46 chronically infected patients. 4Alcohol consumption data before treatment was missing in 18 patients. 5BMI treatment was missing in 215 patients. 6HIV serology was missing in 214 patients. 7Response treatment was assessable in 693 patients. 8Histological activity before treatment was missing in 279 patients. 9Fibrosis stage before treatment was missing in 273 patients. 10Steatosis data before treatment were missing in 155 patients. doi:10.1371/journal.pone.0106424.t001
Summary
Hepatitis C virus (HCV) infects about 2.8% of the global population [1] and is a major cause of chronic liver disease and hepatic mortality worldwide [2,3]. The treatment of HCV genotype 1, the most prevalent in western countries, still relies on the use of pegylated interferon-alpha (IFN-alpha) and ribavirin, with the addition of other direct-acting antivirals [2,3], IFN-alpha-free regimens are currently being registered in several countries and for all viral genotypes [4]. The advent of these welltolerated, highly efficacious drugs will revolutionize HCV screening strategies and the consequent assessment of treatment needs. We explored a possible link between a CCR5 32-base deletion (CCR5delta32), resulting in the expression of a non-functioning receptor, and clinical outcomes of HCV infection
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