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Abstract

Both α- and β-defensins have anti–human immunodeficiency virus activity. These defensins achieve human immunodeficiency virus inhibition through a variety of mechanisms, including direct binding with virions, binding to and modulation of host cell-surface receptors with disruption of intracellular signaling, and functioning as chemokines or cytokines to augment and alter adaptive immune responses. Polymorphisms in the defensin genes have been associated with susceptibility to human immunodeficiency virus infection and disease progression. However, the roles that these defensins and their genetic polymorphisms have in influencing human immunodeficiency virus/acquired immunodeficiency syndrome outcomes are not straightforward and, at times, appear contradictory. Differences in populations, study designs, and techniques for genotyping defensin gene polymorphisms may have contributed to this lack of clarity. In addition, a comprehensive approach, where both subfamilies of defensins and their all-inclusive genetic polymorphism profiles are analyzed, is lacking. Such an approach may reveal whether the human immunodeficiency virus inhibitory activities of α- and β-defensins are based on parallel or divergent mechanisms and may provide further insights into how the genetic predisposition for susceptibility or resistance to human immunodeficiency virus/acquired immunodeficiency syndrome is orchestrated between these molecules.

α-defensins, β-defensins, copy number variation
© 2016 Society for Leukocyte Biology
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
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