Copy Number Variation within Human ÃÂ²-Defensin Gene Cluster Influences Progression to AIDS in the Multicenter AIDS Cohort Study
- *Corresponding Author:
- Richard J. Jurevic
Department of Biological Sciences
Case Western Reserve University School of Dental Medicine
Cleveland, OH 44106-4905, USA
E-mail: [email protected]
Received Date: October 23, 2012; Accepted Date: November 23, 2012; Published Date: November 26, 2012
Citation: Mehlotra RK, Dazard JE, John B, Zimmerman PA, Weinberg A, et al. (2012) Copy Number Variation within Human β-Defensin Gene Cluster Influences Progression to AIDS in the Multicenter AIDS Cohort Study. J AIDS Clinic Res 3:184. doi:10.4172/2155-6113.1000184
Copyright: © 2012 Mehlotra RK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Study background: DEFB4/103A encoding β-defensin 2 and 3, respectively, inhibit CXCR4-tropic (X4) viruses in vitro. We determined whether DEFB4/103A Copy Number Variation (CNV) influences time-to-X4 and time-to-AIDS outcomes. Methods: We utilized samples from a previously published Multicenter AIDS Cohort Study (MACS), which provides longitudinal account of viral tropism in relation to the full spectrum of rates of disease progression. Using traditional models for time-to-event analysis, we investigated association between DEFB4/103A CNV and the two outcomes, and interaction between DEFB4/103A CNV and disease progression groups, Fast and Slow. Results: Time-to-X4 and time-to-AIDS were weakly correlated. There was a stronger relationship between these two outcomes for the fast progressors. DEFB4/103A CNV was associated with time-to-AIDS, but not time-to-X4. The association between higher DEFB4/103A CNV and time-to-AIDS was more pronounced for the slow progressors. Conclusion: DEFB4/103A CNV was associated with time-to-AIDS in a disease progression group-specific manner in the MACS cohort. Our findings may contribute to enhancing current understanding of how genetic predisposition influences AIDS progression.