Indian Journal of Dermatology
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BASIC RESEARCH
Year : 2019  |  Volume : 64  |  Issue : 3  |  Page : 182-186

Evaluation of HCP5 and Chemokine C receptor type 5 gene polymorphisms in Indian psoriatic patients


Department of Cell Biology and Molecular Genetics, Sri Devaraj Urs Academy of Higher Education and Research, Kolar, Karnataka, India

Correspondence Address:
Dr. Sharath Balakrishna
Department of Cell Biology and Molecular Genetics, Sri Devaraj Urs Academy of Higher Education and Research, Tamaka, Kolar - 563 103, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijd.IJD_285_18

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Background: Genetic variations associated with nonprogression of HIV infection to AIDS are enriched in psoriasis patients. HCP5 gene 335 T > G and chemokine C receptor type 5 (CCR5) gene Δ32 polymorphisms are associated with HIV nonprogression phenotype. Aim: The aim of this study was to determine the association of HCP5 gene 335 T > G (rs2395029) and CCR5 gene Δ32 (rs333) polymorphisms with psoriasis vulgaris (PV). Materials and Methods: Genotype of HCP5 gene 335 T > G and CCR5 gene Δ32 polymorphisms were determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism and allele-specific PCR methods, respectively. Results: The frequency of HCP5 gene 335 T > G SNP was ~7 times higher in PV patients than in the control group (P = 1.49 × 10–8; odds ratio [OR] = 10.2; 0.95 confidence interval [CI]: 3.9–26.8). OR for the occurrence of HCP5 335 G allele in either homozygous or heterozygous genotype in PV patients was 13.1 (0.95 CI: 4.7–36.1). The strength of association was higher with moderate-to-severe subgroup (P = 3.29 × 10–9; OR = 18.4; 0.95 CI: 6.2–54.9) than with mild subgroup (P = 2.1 × 10–4; OR = 8.3; 0.95 CI: 2.6–23.3). In addition, the strength of association was higher with Type I (P = 9.53 × 10–8; OR = 15.3; 0.95 CI: 5.1–46.5) than with Type II subgroup (P = 6.8 × 10–6; OR = 11.0; 0.95 CI: 3.6–33.9). Type I gene Δ32 polymorphism was observed neither among psoriatic nor among healthy individuals. Conclusions: Our results indicate that HCP5 gene 335 T > G polymorphism and not CCR5 gene Δ32 polymorphism is associated with the increased risk of developing PV.


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