Abstract
We explored the impact of human ABO glycosyltransferase and Lewis and secretor fucosyltransferase polymorphisms in HIV infection. We found that, compared with healthy blood donors, HIV-infected patients display a significant decrease in Le(a-b+) phenotype frequencies. We showed that HIV binding on DC-SIGN-transduced Jurkat cells was inhibited by fucosyl bovine serum albumin. Our results suggest a slight protective effect of Lewis b antigen on HIV infection, possibly by the competition of Lewis antigens with HIV for binding to DC-SIGN.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Adhesion Molecules / metabolism*
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Fucosyltransferases / genetics*
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HIV Infections / blood*
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HIV Infections / genetics
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Humans
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Jurkat Cells / metabolism
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Lectins, C-Type / metabolism*
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Lewis Blood Group Antigens / genetics*
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Phenotype
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RNA, Viral / metabolism
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Receptors, Cell Surface / metabolism*
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Serum Albumin / metabolism
Substances
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Cell Adhesion Molecules
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DC-specific ICAM-3 grabbing nonintegrin
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Lectins, C-Type
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Lewis Blood Group Antigens
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RNA, Viral
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Receptors, Cell Surface
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Serum Albumin
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Fucosyltransferases