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Human immunodeficiency virus strains differ in their ability to infect CD4+ cells expressing the rat homolog of CXCR-4 (fusin).

Abstract
A clade B strain of human immunodeficiency virus type 1 (HIV-1(LAI)) could infect CD4+ cells expressing human CXCR-4 (fusin) or its rat homolog with similar efficacy. By contrast, cells expressing rat CXCR-4 were not permissive to HIV-1(NDK) (clade D), HIV-2(ROD), or HIV-1(LAI) with chimeric envelope protein gp120 bearing the V3 domain from HIV-1(NDK). The reciprocal chimeric gp120 (HIV-1(NDK) with V3 from HIV-1(LAI)) could mediate infection of cells expressing either human or rat CXCR-4. Genetically divergent HIV strains have different requirements for interaction with the CXCR-4 coreceptor, and the gp120 V3 domain seems to be involved in this interaction.
AuthorsO Pleskoff, N Sol, B Labrosse, M Alizon
JournalJournal of virology (J Virol) Vol. 71 Issue 4 Pg. 3259-62 (Apr 1997) ISSN: 0022-538X [Print] United States
PMID9060691 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • HIV Core Protein p24
  • HIV Envelope Protein gp120
  • HIV envelope protein gp120 (305-321)
  • Membrane Proteins
  • Peptide Fragments
  • Receptors, CXCR4
  • Receptors, HIV
  • Recombinant Fusion Proteins
Topics
  • Animals
  • CD4-Positive T-Lymphocytes (metabolism, virology)
  • HIV Core Protein p24 (analysis)
  • HIV Envelope Protein gp120 (genetics, immunology)
  • HIV-1 (classification, genetics, physiology)
  • HIV-2 (classification, physiology)
  • HeLa Cells
  • Humans
  • Membrane Proteins (biosynthesis, genetics, physiology)
  • Peptide Fragments (genetics, immunology)
  • Rats
  • Receptors, CXCR4
  • Receptors, HIV (biosynthesis, genetics, physiology)
  • Recombinant Fusion Proteins (genetics)
  • Species Specificity
  • Tumor Cells, Cultured

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