Trans-Activator Gene of HTLV-II Induces IL-2 Receptor and IL-2 Cellular Gene Expression

The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1986-05, Vol.232 (4752), p.877-880
Main Authors: Greene, Warner C., Leonard, Warren J., Wano, Yuji, Svetlik, Penny B., Peffer, Nancy J., Sodroski, Joseph G., Rosen, Craig A., Goh, Wei Chun, Haseltine, William A.
Format: Article
Language:English
Subjects:
AIDS/HIV
B lymphocytes
Biochemistry
Biological and medical sciences
Cancer
Cell Line
Cell lines
Deltaretrovirus - genetics
Epithelial cells
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Genes
Genes, Viral
Genetics
Human T lymphotropic virus 1
Human T lymphotropic virus 2
Humans
Interleukin-2
Interleukin-2 - biosynthesis
Interleukin-2 - genetics
Interleukins
Leukemia - microbiology
Medical research
Messenger RNA
Microbiology
Nucleic Acid Hybridization
Plasmids
Receptors
Receptors, Immunologic - genetics
Receptors, Interleukin-2
Retroviruses
RNA, Messenger - genetics
T cells
T lymphocytes
Viral research
Virology
Virus research
Viruses
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Summary:The human T-lymphotropic viruses types I and II (HTLV-I and -II) have been etiologically linked with certain T-cell leukemias and lymphomas that characteristically display membrane receptors for interleukin-2. The relation of these viruses to this growth factor receptor has remained unexplained. It is demonstrated here that introduction of the trans-activator (tat) gene of HTLV-II into the Jurkat T-lymphoid cell line results in the induction of both interleukin-2 receptor and interleukin-2 gene expression. The coexpression of these cellular genes may play a role in the altering T-cell growth following retroviral infection.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.3010456