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CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism.

Publication ,  Journal Article
Chen, CH; Weinhold, KJ; Bartlett, JA; Bolognesi, DP; Greenberg, ML
Published in: AIDS Res Hum Retroviruses
November 1993

HIV-1 infection evokes a vigorous antiviral response that may participate in resolving the initial peak of plasma viremia and maintenance of the asymptomatic state. CD8+ T lymphocytes of HIV-1-infected individuals play a critical role in the cellular anti-HIV response. In agreement with previous reports, we observed a potent suppressive effect on HIV-1 production from autologous CD4+ T lymphocytes by CD8+ T lymphocytes from asymptomatic HIV-1-infected individuals. To elucidate the mechanism(s) of the nonlytic suppressive antiviral activity, we examined the effect of CD8+ T lymphocytes on the transcriptional activity of the HIV-1 promoter (HIV-LTR). CD8+ lymphocytes from HIV-1-infected asymptomatic individuals suppressed tat-mediated HIV-LTR transcription in CD4+ lymphocytes. HIV-LTR transcriptional activity was suppressed by CD8 lymphocytes to an extent similar to tat-mediated transcription whereas CMV immediate early gene promoter activity was not affected. In contrast to the suppressive effect seen with CD8+ lymphocytes from HIV-1-infected individuals, CD8+ lymphocytes from uninfected individuals did not significantly inhibit tat-mediated or HIV-LTR transcription. The transcriptional inhibitory activity was not MHC class I restricted and could be mediated by a soluble factor(s). Supernatants from some CD8+ T lymphocyte cultures from HIV-1+ individuals exerted an inhibitory effect on tat-mediated HIV-LTR transcription comparable to that seen with CD8+ cells. In conclusion, CD8+ lymphocytes from asymptomatic HIV-1+ individuals could suppress virus production by inhibiting HIV-1 gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Duke Scholars

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Published In

AIDS Res Hum Retroviruses

DOI

ISSN

0889-2229

Publication Date

November 1993

Volume

9

Issue

11

Start / End Page

1079 / 1086

Location

United States

Related Subject Headings

  • Virus Replication
  • Virology
  • Transcription, Genetic
  • T-Lymphocyte Subsets
  • Humans
  • Histocompatibility Antigens Class I
  • HIV-1
  • HIV Long Terminal Repeat
  • Cells, Cultured
  • CD8 Antigens
 

Citation

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Chen, C. H., Weinhold, K. J., Bartlett, J. A., Bolognesi, D. P., & Greenberg, M. L. (1993). CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism. AIDS Res Hum Retroviruses, 9(11), 1079–1086. https://doi.org/10.1089/aid.1993.9.1079
Chen, C. H., K. J. Weinhold, J. A. Bartlett, D. P. Bolognesi, and M. L. Greenberg. “CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism.AIDS Res Hum Retroviruses 9, no. 11 (November 1993): 1079–86. https://doi.org/10.1089/aid.1993.9.1079.
Chen CH, Weinhold KJ, Bartlett JA, Bolognesi DP, Greenberg ML. CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism. AIDS Res Hum Retroviruses. 1993 Nov;9(11):1079–86.
Chen, C. H., et al. “CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism.AIDS Res Hum Retroviruses, vol. 9, no. 11, Nov. 1993, pp. 1079–86. Pubmed, doi:10.1089/aid.1993.9.1079.
Chen CH, Weinhold KJ, Bartlett JA, Bolognesi DP, Greenberg ML. CD8+ T lymphocyte-mediated inhibition of HIV-1 long terminal repeat transcription: a novel antiviral mechanism. AIDS Res Hum Retroviruses. 1993 Nov;9(11):1079–1086.
Journal cover image

Published In

AIDS Res Hum Retroviruses

DOI

ISSN

0889-2229

Publication Date

November 1993

Volume

9

Issue

11

Start / End Page

1079 / 1086

Location

United States

Related Subject Headings

  • Virus Replication
  • Virology
  • Transcription, Genetic
  • T-Lymphocyte Subsets
  • Humans
  • Histocompatibility Antigens Class I
  • HIV-1
  • HIV Long Terminal Repeat
  • Cells, Cultured
  • CD8 Antigens