Human immunodeficiency virus long terminal repeat responds to T-cell activation signals.

S. E. Tong-Starksen, Paul A Luciw, B. M. Peterlin

Research output: Contribution to journalArticle

178 Citations (Scopus)

Abstract

Human immunodeficiency virus (HIV), the causative agent of AIDS, infects and kills lymphoid cells bearing the CD4 antigen. In an infected cell, a number of cellular as well as HIV-encoded gene products determine the levels of viral gene expression and HIV replication. Efficient HIV-replication occurs in activated T cells. Utilizing transient expression assays, we show that gene expression directed by the HIV long terminal repeat (LTR) increases in response to T-cell activation signals. The effects of T-cell activation and of the HIV-encoded trans-activator (TAT) are multiplicative. Analysis of mutations and deletions in the HIV LTR reveals that the region responding to T-cell activation signals is located at positions -105 to -80. These sequences are composed of two direct repeats, which are homologous to the core transcriptional enhancer elements in the simian virus 40 genome. Our studies reveal that these elements function as the HIV enhancer. By acting directly on the HIV LTR, T-cell activation may play an important role in HIV gene expression and in the activation of latent HIV.

Original languageEnglish (US)
Pages (from-to)6845-6849
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume84
Issue number19
StatePublished - Oct 1987
Externally publishedYes

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HIV Long Terminal Repeat
HIV
T-Lymphocytes
Virus Replication
Gene Expression
Human Immunodeficiency Virus Proteins
CD4 Antigens
Trans-Activators
Simian virus 40
Viral Genes
Sequence Deletion
Nucleic Acid Repetitive Sequences
Acquired Immunodeficiency Syndrome
Cell Count
Genome
Lymphocytes

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Human immunodeficiency virus long terminal repeat responds to T-cell activation signals. / Tong-Starksen, S. E.; Luciw, Paul A; Peterlin, B. M.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 84, No. 19, 10.1987, p. 6845-6849.

Research output: Contribution to journalArticle

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