Gastroenterology

Gastroenterology

Volume 124, Issue 3, March 2003, Pages 867-868
Gastroenterology

Correspondence
High frequency of CCR5-Δ32 homozygosity in HCV-infected, HIV-1-uninfected hemophiliacs results from resistance to HIV-1

https://doi.org/10.1053/gast.2003.50132Get rights and content

Abstract

GASTROENTEROLOGY 2003;124:867-868

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Dear Sir:

CCR5-Δ32 homozygotes are resistant to infection by human immunodeficiency virus type 1 (HIV-1)1, 2, 3 because they do not express CCR5, which is a major HIV-1 coreceptor.4, 5, 6, 7 Wiotas et al.8 recently reported that the CCR5-Δ32 homozygous genotype was increased in 153 patients who were infected with hepatitis C virus (HCV) but not HIV-1. They also found that HCV-infected, HIV-1-uninfected subjects with the CCR5-Δ32 homozygous genotype had higher HCV levels than CCR5 wild-type patients.8

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    Considering that the CCR5Δ32 homozygous genotype provides protection against HIV infection, a high frequency of this genotype in an HCV-infected group may be due to HIV resistance, but not to HCV, among individuals highly exposed to both viruses. Due to those and other reasons, the results of Woitas et al. (2002) were criticized by different authors (Klein, 2003; Mangia et al., 2003; Poljak et al., 2003; Promrat et al., 2003; Zhang et al., 2003). In this sense, no influence of CCR5Δ32 on susceptibility to HCV infection were reported in studies performed with various populations (Glas et al., 2003; Mangia et al., 2003; Poljak et al., 2003; Promrat et al., 2003; Zhang et al., 2003; Ruiz-Ferrer et al., 2004; Wald et al., 2004; Wasmuth et al., 2004; Thoelen et al., 2005; Goyal et al., 2006).

  • CCR5Δ32 in HCV infection, HCV/HIV co-infection, and HCV-related diseases

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    In this same study, HCV/HIV co-infected individuals also showed a higher frequency of the Δ32 allele compared to HIV mono-infected patients (Woitas et al., 2002). Although it is true that this work drew attention to the potential roles of CCR5 and CCR5Δ32 on the susceptibility to HCV infection and HCV-related diseases, due to potential confounding situations (i.e. high number of hemophiliac patients included, among others), it has generated a great debate (Klein, 2003; Mangia et al., 2003; Poljak et al., 2003; Zhang et al., 2003). In line with the criticisms made regarding this study conclusions, our results do not support an influence of the CCR5Δ32 allele on the susceptibility to HCV infection or HCV/HIV co-infection in the Brazilian population.

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    Interestingly, a common 32-base deletion in the CCR5 gene has been associated with resistance to HIV-1 infection [86–88]. The potential role of CCR5 deletion in resistance to HCV has been studied and suggested to adversely affect outcome of HCV infection [89–94]. However, the different reports are conflicting.

  • The predictive value of IL28B gene polymorphism for spontaneous clearance in a single source outbreak cohort is limited in patients carrying the CCR5Δ32 mutation

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    It has been proposed that CCR5Δ32 homozygosity might be a risk factor for a chronic course in hepatitis C infection [33] also heralding a poor response to interferon therapy [34]. However, this putative association between CCR5Δ32 and chronic hepatitis C was not confirmed in subsequent studies [35–46]. Discrepancies between the various studies could not be resolved and effects from uncontrolled confounding factors, e.g. selection pressure due to concomitant HIV exposure, have been incriminated.

  • CXCR3 expression on peripheral CD4<sup>+</sup> T cells as a predictive marker of response to treatment in chronic hepatitis C

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