Abstract
Changes in co-receptor-use by human immunodeficiency virus type 1 (HIV-1) strains are relatively rare in vivo. Here we describe two variants derived from the CCR5-using strain SF162, selected for replication in the C8166 T-cell line. Amino acid substitutions in the V3 loop conferred CXCR4-use; however, the loss of macrophage-tropism by one variant was due to a single mutation in the start codon of vpu. We discuss how V3 loop and vpu mutations acquired by replication in T-cell lines in vitro correlate with similar changes reported for primary isolates and HIV-1 sequences in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptation, Physiological*
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Amino Acid Sequence
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Base Sequence
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Cell Line
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Cloning, Molecular
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Codon, Initiator / genetics
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DNA, Recombinant / genetics
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DNA, Viral / genetics
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Genetic Variation / genetics
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HIV / chemistry
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HIV / genetics*
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HIV / metabolism
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HIV / physiology*
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HIV Envelope Protein gp160 / chemistry
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HIV Envelope Protein gp160 / genetics*
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HIV Envelope Protein gp160 / metabolism
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Human Immunodeficiency Virus Proteins
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Humans
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Macrophages / metabolism
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Macrophages / virology*
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Molecular Sequence Data
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Receptors, CCR5 / metabolism
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Receptors, CXCR4 / metabolism
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Sequence Alignment
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Serial Passage
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T-Lymphocytes / metabolism
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T-Lymphocytes / virology*
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Viral Regulatory and Accessory Proteins / chemistry
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Viral Regulatory and Accessory Proteins / genetics*
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Viral Regulatory and Accessory Proteins / physiology
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Virus Replication
Substances
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Codon, Initiator
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DNA, Recombinant
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DNA, Viral
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HIV Envelope Protein gp160
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Human Immunodeficiency Virus Proteins
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Receptors, CCR5
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Receptors, CXCR4
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Viral Regulatory and Accessory Proteins
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vpu protein, Human immunodeficiency virus 1