BACKGROUND: The genotypic polymorphisms of CCR5, CCR2, and SDF1 were analyzed to determine their impact as potential confounders with regard to disease progression because of the role that host genetic factors appear to be involved in determining rates of disease progression. METHODS: Genomic DNA was extracted from Ethylenediaminetetraacetate whole blood using Qiagen DNA extraction kit. The amplification of CCR5, CCR2, and SDF1 genes was performed by PCR. RESULTS: Two hundred and twenty-one samples were genotyped for the CCR5, CCR2, and SDF1 mutation. Among these, all (100%) were identified as wild type for CCR5. All were then investigated considering the impact on CD4+ T-cell counts. Samples were divided into two groups based on the CD4+ T-cell numbers. It revealed that in the group of CD4+ T-cell counts ≥200 cells/μl, 15 were found for the homozygous for SDF1 gene (3'A/3'A) whereas one was found in the group of CD4+ T-cell counts <200 cells/μl. Homozygosity for the CCR2 polymorphisms (64I/64I) were five in the group of CD4+ T-cell counts ≥200 cells/μl and none were found in the group of CD4+ T-cell counts <200 cells/μl. These results demonstrated that there was a significant association between CD4+ T-cell numbers and CCR2 and SDF1 polymorphisms (P < 0.001). CONCLUSIONS: The mutation of CCR2 and SDF1 genes showed a significant difference in the distribution of CD4+ T-cell numbers (P < 0.001) whereas mutation of chemokine coreceptor CCR5 was not appeared to be associated with the impact of CD4+ T-cell counts.
BACKGROUND: The genotypic polymorphisms of CCR5, CCR2, and SDF1 were analyzed to determine their impact as potential confounders with regard to disease progression because of the role that host genetic factors appear to be involved in determining rates of disease progression. METHODS: Genomic DNA was extracted from Ethylenediaminetetraacetate whole blood using Qiagen DNA extraction kit. The amplification of CCR5, CCR2, and SDF1 genes was performed by PCR. RESULTS: Two hundred and twenty-one samples were genotyped for the CCR5, CCR2, and SDF1 mutation. Among these, all (100%) were identified as wild type for CCR5. All were then investigated considering the impact on CD4+ T-cell counts. Samples were divided into two groups based on the CD4+ T-cell numbers. It revealed that in the group of CD4+ T-cell counts ≥200 cells/μl, 15 were found for the homozygous for SDF1 gene (3'A/3'A) whereas one was found in the group of CD4+ T-cell counts <200 cells/μl. Homozygosity for the CCR2 polymorphisms (64I/64I) were five in the group of CD4+ T-cell counts ≥200 cells/μl and none were found in the group of CD4+ T-cell counts <200 cells/μl. These results demonstrated that there was a significant association between CD4+ T-cell numbers and CCR2 and SDF1 polymorphisms (P < 0.001). CONCLUSIONS: The mutation of CCR2 and SDF1 genes showed a significant difference in the distribution of CD4+ T-cell numbers (P < 0.001) whereas mutation of chemokine coreceptor CCR5 was not appeared to be associated with the impact of CD4+ T-cell counts.
Authors: M W Smith; M Dean; M Carrington; C Winkler; G A Huttley; D A Lomb; J J Goedert; T R O'Brien; L P Jacobson; R Kaslow; S Buchbinder; E Vittinghoff; D Vlahov; K Hoots; M W Hilgartner; S J O'Brien Journal: Science Date: 1997-08-15 Impact factor: 47.728
Authors: Jianming Tang; Brent Shelton; Nina J Makhatadze; Yuting Zhang; Margaret Schaen; Leslie G Louie; James J Goedert; Eric C Seaberg; Joseph B Margolick; John Mellors; Richard A Kaslow Journal: J Virol Date: 2002-01 Impact factor: 5.103
Authors: J P Ioannidis; P S Rosenberg; J J Goedert; L J Ashton; T L Benfield; S P Buchbinder; R A Coutinho; J Eugen-Olsen; T Gallart; T L Katzenstein; L G Kostrikis; H Kuipers; L G Louie; S A Mallal; J B Margolick; O P Martinez; L Meyer; N L Michael; E Operskalski; G Pantaleo; G P Rizzardi; H Schuitemaker; H W Sheppard; G J Stewart; I D Theodorou; H Ullum; E Vicenzi; D Vlahov; D Wilkinson; C Workman; J F Zagury; T R O'Brien Journal: Ann Intern Med Date: 2001-11-06 Impact factor: 25.391
Authors: C Winkler; W Modi; M W Smith; G W Nelson; X Wu; M Carrington; M Dean; T Honjo; K Tashiro; D Yabe; S Buchbinder; E Vittinghoff; J J Goedert; T R O'Brien; L P Jacobson; R Detels; S Donfield; A Willoughby; E Gomperts; D Vlahov; J Phair; S J O'Brien Journal: Science Date: 1998-01-16 Impact factor: 47.728
Authors: L G Kostrikis; Y Huang; J P Moore; S M Wolinsky; L Zhang; Y Guo; L Deutsch; J Phair; A U Neumann; D D Ho Journal: Nat Med Date: 1998-03 Impact factor: 53.440
Authors: Stephanie A Mulherin; Thomas R O'Brien; John P Ioannidis; James J Goedert; Susan P Buchbinder; Roel A Coutinho; Beth D Jamieson; Laurence Meyer; Nelson L Michael; Giuseppe Pantaleo; G Paolo Rizzardi; Hanneke Schuitemaker; Haynes W Sheppard; Ioannis D Theodorou; David Vlahov; Philip S Rosenberg Journal: AIDS Date: 2003-02-14 Impact factor: 4.177
Authors: M Parczewski; M Leszczyszyn-Pynka; M Kaczmarczyk; G Adler; A Binczak-Kuleta; B Loniewska; A Boron-Kaczmarska; A Ciechanowicz Journal: J Appl Genet Date: 2009 Impact factor: 2.653