Differential Regulation of HIV-1 Fusion Cofactor Expression by CD28 Costimulation of CD4 + T Cells

Author:

Carroll Richard G.12345,Riley James L.12345,Levine Bruce L.12345,Feng Yu12345,Kaushal Sumesh12345,Ritchey David W.12345,Bernstein Wendy12345,Weislow Owen S.12345,Brown Charles R.12345,Berger Edward A.12345,June Carl H.12345,St. Louis Daniel C.12345

Affiliation:

1. R. G. Carroll, S. Kaushal, D. W. Ritchey, D. C. St. Louis, Henry M. Jackson Foundation for the Advancement of Military Medicine, Rockville, MD 20850, USA.

2. J. L. Riley and W. Bernstein, Division of Retrovirology, Walter Reed Army Institute for Research, Rockville, MD 20850, USA.

3. B. L. Levine, Immune Cell Biology Program, Naval Medical Research Institute, Bethesda, MD 20889, USA.

4. Y. Feng and E. A. Berger, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

5. O. S. Weislow, Life Sciences Division, SRA Technologies, Rockville, MD 20850, USA.

Abstract

Activation of CD4 + T lymphocytes from human immunodeficiency virus–type 1 (HIV-1)–infected donors with immobilized antibodies to CD3 and CD28 induces a virus-resistant state. This effect is specific for macrophage-tropic HIV-1. Transcripts encoding CXCR4/Fusin, the fusion cofactor used by T cell line–tropic isolates, were abundant in CD3/CD28-stimulated cells, but transcripts encoding CCR5, the fusion cofactor used by macrophage-tropic viruses, were not detectable. Thus, CD3/CD28 costimulation induces an HIV-1–resistant phenotype similar to that seen in some highly exposed and HIV-uninfected individuals.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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