Abstract
Experiments to identify cell determinants involved in HIV-1 tropism revealed a specific decrease in the expression of the T-cell activation antigen CD26 after monocytotropic (M-tropic) but not T-cell line-tropic (T-tropic) virus infection of the PM1 T-cell line. The level of CD26 expression in single-cell clones of PM1 correlated with the entry rate and cytopathicity of M-tropic HIV-1 variants, resulting in preferential survival of cells with low CD26 levels after infection. Experiments with recombinant viruses showed that the third hypervariable region of the envelope gp120 plays an important role in this selection process. This study identifies CD26 as a key marker for M-tropic human immunodeficiency virus type 1 (HIV-1) infection and suggests a mechanism for the early loss of CD26-expressing cells in HIV-1-infected individuals.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Base Sequence
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CD4-Positive T-Lymphocytes / enzymology
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CD4-Positive T-Lymphocytes / virology*
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Cell Survival
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Cells, Cultured
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Cytopathogenic Effect, Viral
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DNA, Viral / analysis
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Dipeptidyl Peptidase 4 / biosynthesis
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Dipeptidyl Peptidase 4 / genetics
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Dipeptidyl Peptidase 4 / physiology*
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Down-Regulation
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Gene Expression Regulation, Viral
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HIV Envelope Protein gp120 / metabolism
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HIV Infections / immunology
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HIV Infections / pathology
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HIV Infections / virology
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HIV-1 / pathogenicity
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HIV-1 / physiology*
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Humans
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Molecular Sequence Data
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Monocytes / virology
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Peptide Fragments / metabolism
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RNA, Messenger / biosynthesis
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Receptors, Virus*
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Virus Replication
Substances
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DNA, Viral
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HIV Envelope Protein gp120
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HIV envelope protein gp120 (305-321)
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Peptide Fragments
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RNA, Messenger
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Receptors, Virus
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Dipeptidyl Peptidase 4