BACKGROUND & AIMS: A homozygous 32-base pair deletion in the CCR5 gene (CCR5-Delta32) protects against human immunodeficiency virus infection (HIV). However, the role of this mutation in other infections, such as hepatitis C virus (HCV) infection, has not been defined. METHODS: We determined the frequency of the CCR5-Delta32 mutation by polymerase chain reaction in anti-HCV(+) (n = 153), anti-HIV(+) (n = 102), and anti-HCV(+)/HIV(+) (n = 130) white patients as well as in 102 healthy blood donors. Then, HIV and HCV loads, aminotransferases, and CD4 and CD8 cell counts were compared between the resulting subsets of CCR5-Delta32/wild-type heterozygotes, CCR5-Delta32, and wild-type homozygotes, respectively. RESULTS: Twelve of 153 (7.8%) anti-HCV-seropositive patients and 1 of 102 (1.0%) healthy blood donors were CCR5-Delta32 homozygous, whereas CCR5-Delta32 homozygosity was absent in anti-HIV(+) and anti-HCV(+)/HIV(+) patients (P < 0.001). The frequency of the CCR5-Delta32 allele was higher in the anti-HCV(+) (16.0%, P < 0.05) and anti-HCV(+)/HIV(+) (12.7%, NS) patients than in healthy blood donors (8.3%) and anti-HIV(+) patients (9.3%), respectively. Anti-HCV(+) CCR5-Delta32 homozygotes occurred 3 times more frequently than expected from the Hardy-Weinberg equation (P < 0.0001) and had significantly higher HCV loads than wild-type patients (P = 0.045). CONCLUSIONS: The increased prevalence of CCR5-Delta32 homozygosity associated with increased viral loads in patients with chronic hepatitis C suggests that the CCR5-Delta32 mutation may be an adverse host factor in hepatitis C.
BACKGROUND & AIMS: A homozygous 32-base pair deletion in the CCR5 gene (CCR5-Delta32) protects against human immunodeficiency virus infection (HIV). However, the role of this mutation in other infections, such as hepatitis C virus (HCV) infection, has not been defined. METHODS: We determined the frequency of the CCR5-Delta32 mutation by polymerase chain reaction in anti-HCV(+) (n = 153), anti-HIV(+) (n = 102), and anti-HCV(+)/HIV(+) (n = 130) white patients as well as in 102 healthy blood donors. Then, HIV and HCV loads, aminotransferases, and CD4 and CD8 cell counts were compared between the resulting subsets of CCR5-Delta32/wild-type heterozygotes, CCR5-Delta32, and wild-type homozygotes, respectively. RESULTS: Twelve of 153 (7.8%) anti-HCV-seropositive patients and 1 of 102 (1.0%) healthy blood donors were CCR5-Delta32 homozygous, whereas CCR5-Delta32 homozygosity was absent in anti-HIV(+) and anti-HCV(+)/HIV(+) patients (P < 0.001). The frequency of the CCR5-Delta32 allele was higher in the anti-HCV(+) (16.0%, P < 0.05) and anti-HCV(+)/HIV(+) (12.7%, NS) patients than in healthy blood donors (8.3%) and anti-HIV(+) patients (9.3%), respectively. Anti-HCV(+) CCR5-Delta32 homozygotes occurred 3 times more frequently than expected from the Hardy-Weinberg equation (P < 0.0001) and had significantly higher HCV loads than wild-type patients (P = 0.045). CONCLUSIONS: The increased prevalence of CCR5-Delta32 homozygosity associated with increased viral loads in patients with chronic hepatitis C suggests that the CCR5-Delta32 mutation may be an adverse host factor in hepatitis C.
Authors: Ankur Goyal; P V Suneetha; G T Kumar; Deepak K Shukla; Naveen Arora; Shiv K Sarin Journal: World J Gastroenterol Date: 2006-08-07 Impact factor: 5.742
Authors: S Mascheretti; H Hinrichsen; S Ross; P Buggisch; J Hampe; U R Foelsch; S Schreiber Journal: Clin Exp Immunol Date: 2004-05 Impact factor: 4.330
Authors: Hermann E Wasmuth; Alexa Werth; Tobias Mueller; Thomas Berg; Christoph G Dietrich; Andreas Geier; Ramin Schirin-Sokhan; Carsten Gartung; Johann Lorenzen; Siegfried Matern; Frank Lammert Journal: J Mol Med (Berl) Date: 2003-12-13 Impact factor: 4.599