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1 June 2005

Volume 191, Number 11
The Journal of Infectious Diseases 2005;191:1971–1980
© 2005 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19111-0025$15.00
DOI: 10.1086/430091
MAJOR ARTICLE

Genetic Polymorphisms in CX3CR1 Predict HIV‐1 Disease Progression in Children Independently of CD4+ Lymphocyte Count and HIV‐1 RNA Load

Kumud K. Singh,1

Michael D. Hughes,4

Jie Chen,4 and

Stephen A. Spector1,2,3

1Department of Pediatrics, Division of Infectious Diseases, 2Center for Molecular Genetics, and 3Center for AIDS Research, University of California, San Diego, La Jolla; 4Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts

Background.The impact of CX3CR1 polymorphisms on human immunodeficiency virus type 1 (HIV‐1) pathogenesis is controversial, with conflicting reports of their role in disease progression in HIV‐1–infected adults.

Methods.A cohort of 1055 HIV‐1–infected children were genotyped for 2 CX3CR1 polymorphisms, V/I249 and T/M280, and their impact on HIV‐1–related disease progression, including central nervous system (CNS) impairment, was evaluated.

Results.Children with the CX3CR1 I/I249 genotype experienced more‐rapid disease progression (I/I249 vs. V/V249: relative hazard [RH], 2.19 [95% confidence interval {CI}, 1.30–3.68], ; I/I249 vs. V/I249: RH, 1.77 [95% CI, 1.00–3.14], ) and a trend toward more CNS impairment (I/I249 vs. V/V249: RH, 2.19 [95% CI, 1.00–4.78], ; I/I249 vs. V/I249: RH, 2.02 [95% CI, 0.85–4.83], ). Children with the V249‐T280 haplotype experienced significantly less disease progression (RH, 0.42 [95% CI, 0.24–0.73]; ) and CNS impairment (RH, 0.39 [95% CI, 0.39–0.22]; ). Of note, these effects remained significant after CD4+ lymphocyte count and plasma HIV‐1 RNA load at baseline were adjusted for and in a longitudinal, multivariate analysis.

Conclusions.CX3CR1 genotypes and haplotypes impact HIV‐1 disease progression independently of CD4+ lymphocyte count and plasma HIV‐1 RNA load, suggesting that the fundamental role of CX3CR1 in the alteration of disease progression might be the recruitment of immunomodulatory cells responsible for the control of HIV‐1.

Received 15 October 2004; accepted 13 January 2005; electronically published 28 April 2005.

Reprints or correspondence: Dr. Stephen A. Spector, Dept. of Pediatrics, University of California, San Diego, 9500 Gilman Dr., La Jolla, CA 92093‐0672 ().

Cited by

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Ajay Wanchu, Kumud K Singh. (2008) Function and polymorphisms of anti-HIV host factors: evidence from exposed uninfected individuals. Future HIV Therapy 2:2, 167-173
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A.M. Passam, G. Sourvinos, E. Krambovitis, S. Miyakis, N. Stavrianeas, I. Zagoreos, D.A. Spandidos. (2007) Polymorphisms of Cx3CR1 and CXCR6 Receptors in Relation to HAART Therapy of HIV Type 1 Patients. AIDS Research and Human Retroviruses 23:8, 1026-1032
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Benedicte Puissant, Francis Roubinet, Patrice Massip, Karine Sandres-Saune, Pol-Andre Apoil, Michel Abbal, Christophe Pasquier, Jacques Izopet, Antoine Blancher. (2006) Analysis of CCR5, CCR2, CX3CR1, and SDF1 Polymorphisms in HIV-Positive Treated Patients: Impact on Response to HAART and on Peripheral T Lymphocyte Counts. AIDS Research and Human Retroviruses 22:2, 153-162
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Kumud K Singh, Michael D Hughes, Jie Chen, Stephen A Spector. (2006) Impact of MCP-1-2518-G allele on the HIV-1 disease of children in the United States. AIDS 20:3, 475???478
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Amalio Telenti, Gabriela Bleiber. (2006) Host genetics of HIV-1 susceptibility. Future Virology 1:1, 55-70
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  • Presented in part: XIth Conference on Retroviruses and Opportunistic Infections, San Francisco, 8–11 February 2004 (oral abstract 153).

    Financial support: Pediatric AIDS Clinical Trials Group; National Institute of Allergy and Infectious Diseases (grants AI‐39004, AI‐27563, AI‐33835, AI‐41110, and AI‐36214 [to the Virology Core, University of California, San Diego, Center for AIDS Research]); Rest Haven, San Diego, CA.

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