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Ultraviolet radiation increases HIV-long terminal repeat-directed expression in transgenic mice
D M Frucht1, L Lamperth, E Vicenzi
1Laboratory of Molecular Microbiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
AIDS Research and Human Retroviruses
|September 1, 1991
Summary
UV radiation effectively activates human immunodeficiency virus (HIV) long terminal repeat (LTR) gene expression in mice. UV-C radiation showed a greater induction of HIV-LTR-directed expression compared to UV-B radiation.
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- The human immunodeficiency virus (HIV) long terminal repeat (LTR) is a key regulatory element controlling viral gene expression.
- Understanding factors that modulate HIV-LTR activity is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the effect of ultraviolet (UV) radiation on HIV-LTR-directed gene expression in vivo.
- To compare the efficacy of UV-C and UV-B radiation in inducing HIV-LTR expression.
Main Methods:
- FVB/N mice carrying an HIV-LTR/chloramphenicol acetyl transferase (CAT) transgene were exposed to UV-C (254 nm) or UV-B (312 nm) radiation.
- CAT gene expression levels were measured in ear and skin tissues at various time points post-exposure.
Main Results:
- UV-C exposure resulted in a 20-fold increase in HIV-LTR expression in ear tissue, while UV-B induced a fourfold increase.
- UV-C induction peaked on Day 3 (over 30-fold), and UV-B induction peaked on Day 5 (fivefold).
- CAT activity was not induced in fur-bearing skin but increased fourfold in shaved skin after UV-B treatment.
Conclusions:
- UV radiation, particularly UV-C, can significantly activate HIV-LTR-directed gene expression in mice.
- The presence of fur inhibits UV-induced gene expression, suggesting skin barrier properties influence activation.
- These findings may have implications for understanding viral reactivation and developing targeted therapies.