| Conclusion | Our results seem to indicate that the CCR5-Delta32 and CCR2-V64I polymorphisms are not related to the response to HCV infection, histological damage and outcome of infection in our cohort of Spanish HCV patients.;Differential receptor expression due to E/E homozygosity in HCV infection remains to be confirmed.;The G190A polymorphism (variant allele Ile64) in the first transmembrane domain of CCR2 was under-represented in the 29 patients who had cleared the HuLDi00024 virus spontaneously (P = 0.018). None of the other variants in the CCR gene cluster showed association with the natural course of the infection, stage of fibrosis or response to therapy.;Heterozygosity for CCR5delta32 was shown to be significantly associated with spontaneous HuLDi00024 viral clearance and with significantly lower hepatic inflammatory scores in subgroups within this cohort. Both controls and the HCV population had similar heterozygosity frequencies.;In this cohort, the frequency of CCR5Delta32 homozygosity in patients with HuLDi00024 was similar to controls. The high prevalence of CCR5Delta32 homozygosity in the HuLDi00024 virus patients of the earlier study likely reflects resistance to human immunodeficiency virus infection in hemophiliacs rather than a susceptibility to HuLDi00024. Expression of CCR5 and RANTES may be important in the modulation of hepatic inflammation and response to interferon therapy in HuLDi00025.;Our results indicate that the mutations studied in the gene pair CCL2/CCR2 do not play a major role in the outcome and response to treatment for HCV infection in the Spanish population.Conclusion1 |
