HIV transcription is induced with cell killing
Abstract
Previous work has shown that HeLa cells stably transfected with an HIV-LTR-CAT construct are induced to express chloramphenicol acetyl transferase (CAT) following exposure to DNA-damaging agents such as ultraviolet radiation, {gamma} rays, neutrons, and others. In this report, the authors demonstrate that this induction of HIV-LTR transcription occurs when stably transfected HeLa cells are exposed to agents which mediate cell killing, such as UV radiation, electroporation of sucrose buffer, prolonged heating, and low and high pH. Cells cultured following UV exposure demonstrated a peak in CAT expression that is evidence in viable (but not necessarily cell division-competent) cells 24 h after exposure; this inductive response continued until at least 72 h after exposure. HIV-LTR induction was dose-dependent, and the amount of CAT transcription induced was correlated with the amount of cell killing that occurred in the culture. Other agents which caused no cell killing (such as heat-shock for up to 2 h, treatment with metronidazole, exposure to sunlight, vitamin C treatment, and others) had no effect on HIV-LTR induction. These results suggest that HIV transcription is induced as a consequence of the turn on of a cellular death or apoptotic pathway.
- Authors:
-
- Argonne National Lab., IL (United States)
- Loyola Univ. Medical Center, Maywood, IL (United States). Dept. of Pathology
- Loyola Univ. Medical Center, Maywood, IL (United States)
- Publication Date:
- Research Org.:
- Argonne National Lab., IL (United States)
- Sponsoring Org.:
- USDOE, Washington, DC (United States)
- OSTI Identifier:
- 10114046
- Report Number(s):
- ANL/CMB/PP-81167
ON: DE94005122; TRN: AHC29402%%47
- DOE Contract Number:
- W-31109-ENG-38
- Resource Type:
- Technical Report
- Resource Relation:
- Other Information: PBD: [1994]
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; HELA CELLS; CELL KILLING; AIDS VIRUS; TRANSCRIPTION; RADIOSENSITIVITY; 560120; RADIATION EFFECTS ON BIOCHEMICALS, CELLS, AND TISSUE CULTURE
Citation Formats
Woloschak, G E, Schreck, S, Chang-Liu, Chin Mei, Panozzo, J, and Libertin, C R. HIV transcription is induced with cell killing. United States: N. p., 1994.
Web.
Woloschak, G E, Schreck, S, Chang-Liu, Chin Mei, Panozzo, J, & Libertin, C R. HIV transcription is induced with cell killing. United States.
Woloschak, G E, Schreck, S, Chang-Liu, Chin Mei, Panozzo, J, and Libertin, C R. 1994.
"HIV transcription is induced with cell killing". United States.
@article{osti_10114046,
title = {HIV transcription is induced with cell killing},
author = {Woloschak, G E and Schreck, S and Chang-Liu, Chin Mei and Panozzo, J and Libertin, C R},
abstractNote = {Previous work has shown that HeLa cells stably transfected with an HIV-LTR-CAT construct are induced to express chloramphenicol acetyl transferase (CAT) following exposure to DNA-damaging agents such as ultraviolet radiation, {gamma} rays, neutrons, and others. In this report, the authors demonstrate that this induction of HIV-LTR transcription occurs when stably transfected HeLa cells are exposed to agents which mediate cell killing, such as UV radiation, electroporation of sucrose buffer, prolonged heating, and low and high pH. Cells cultured following UV exposure demonstrated a peak in CAT expression that is evidence in viable (but not necessarily cell division-competent) cells 24 h after exposure; this inductive response continued until at least 72 h after exposure. HIV-LTR induction was dose-dependent, and the amount of CAT transcription induced was correlated with the amount of cell killing that occurred in the culture. Other agents which caused no cell killing (such as heat-shock for up to 2 h, treatment with metronidazole, exposure to sunlight, vitamin C treatment, and others) had no effect on HIV-LTR induction. These results suggest that HIV transcription is induced as a consequence of the turn on of a cellular death or apoptotic pathway.},
doi = {},
url = {https://www.osti.gov/biblio/10114046},
journal = {},
number = ,
volume = ,
place = {United States},
year = {Sat Jan 01 00:00:00 EST 1994},
month = {Sat Jan 01 00:00:00 EST 1994}
}