Abstract
The compound genotype KIR3DS1/HLA-B Bw4-80I, which presumably favors natural killer cell activation, has been implicated in protection against HIV disease. We show that this genotype confers dual protection over the course of HIV disease; early direct containment of HIV viral load, and late specific defense against opportunistic infections, but not AIDS-related malignancies. The double protection of KIR3DS1/Bw4-80I in an etiologically complex disease such as AIDS, along with the disease specificity of its effects is conceptually novel and underscores the intricacy of host immunogenetics against HIV/AIDS.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, N.I.H., Intramural
MeSH terms
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AIDS-Related Opportunistic Infections / genetics*
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AIDS-Related Opportunistic Infections / immunology
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Acquired Immunodeficiency Syndrome / genetics*
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Acquired Immunodeficiency Syndrome / immunology
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Disease Progression
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HIV Seropositivity
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HIV-1
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HLA-B Antigens / genetics*
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HLA-B Antigens / immunology
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Humans
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Immunocompromised Host
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Immunosuppression Therapy
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Killer Cells, Natural / immunology*
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Killer Cells, Natural / virology
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Lymphoma, AIDS-Related / genetics
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Lymphoma, AIDS-Related / immunology
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Receptors, Immunologic / genetics*
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Receptors, Immunologic / immunology
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Receptors, KIR
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Receptors, KIR3DS1
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Sarcoma, Kaposi / genetics
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Sarcoma, Kaposi / immunology
Substances
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HLA-B Antigens
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Receptors, Immunologic
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Receptors, KIR
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Receptors, KIR3DS1