This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ariumi, Y.
Right arrow Articles by Trono, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ariumi, Y.
Right arrow Articles by Trono, D.

 Previous Article  |  Next Article 

Journal of Virology, March 2005, p. 2973-2978, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2973-2978.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

DNA Damage Sensors ATM, ATR, DNA-PKcs, and PARP-1 Are Dispensable for Human Immunodeficiency Virus Type 1 Integration

Yasuo Ariumi,1 Priscilla Turelli,1 Mitsuko Masutani,2 and Didier Trono1*

Department of Microbiology and Molecular Medicine and "Frontiers in Genetics" Research Program, Faculty of Medicine, University of Geneva, Geneva, Switzerland,1 Biochemistry Division, National Cancer Center Research Institute, Tokyo, Japan2

Received 13 August 2004/ Accepted 8 October 2004

Integration of a DNA copy of the viral RNA genome is a crucial step in the life cycle of human immunodeficiency virus type 1 (HIV-1) and other retroviruses. While the virally encoded integrase is key to this process, cellular factors yet to be characterized are suspected to participate in its completion. DNA damage sensors such as ATM (ataxia-telangiectasia mutated), ATR (ATM- and Rad3-related), DNA-PK (DNA-dependent protein kinase), and PARP-1 [poly(ADP-ribose) polymerase 1] play central roles in responses to various forms of DNA injury and as such could facilitate HIV integration. To test this hypothesis, we examined the susceptibility to infection with wild-type HIV-1 and to transduction with a vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1-derived lentiviral vector of human cells stably expressing small interfering RNAs against ATM, ATR, and PARP-1. We found that integration normally occurred in these knockdown cells. Similarly, the VSV-G-pseudotyped HIV-1-based vector could effectively transduce ATM and PARP-1 knockout mouse cells as well as human cells deficient for DNA-PK. Finally, treatment of target cells with the ATM and ATR inhibitors caffeine and wortmannin was without effect in these infectivity assays. We conclude that the DNA repair enzymes ATM, ATR, DNA-PKcs, and PARP-1 are not essential for HIV-1 integration.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva, 1211, Geneva 4, Switzerland. Phone: 41-22-379 5720. Fax: 41-22-379 5721. E-mail: Didier.trono{at}medecine.unige.ch.

Journal of Virology, March 2005, p. 2973-2978, Vol. 79, No. 5
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.5.2973-2978.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kuroki, M., Ariumi, Y., Ikeda, M., Dansako, H., Wakita, T., Kato, N. (2009). Arsenic Trioxide Inhibits Hepatitis C Virus RNA Replication through Modulation of the Glutathione Redox System and Oxidative Stress. J. Virol. 83: 2338-2348 [Abstract] [Full Text]  
  • Ariumi, Y., Kuroki, M., Dansako, H., Abe, K.-I., Ikeda, M., Wakita, T., Kato, N. (2008). The DNA Damage Sensors Ataxia-Telangiectasia Mutated Kinase and Checkpoint Kinase 2 Are Required for Hepatitis C Virus RNA Replication. J. Virol. 82: 9639-9646 [Abstract] [Full Text]  
  • Curcio, M. J., Kenny, A. E., Moore, S., Garfinkel, D. J., Weintraub, M., Gamache, E. R., Scholes, D. T. (2007). S-Phase Checkpoint Pathways Stimulate the Mobility of the Retrovirus-Like Transposon Ty1. Mol. Cell. Biol. 27: 8874-8885 [Abstract] [Full Text]  
  • Ariumi, Y., Kuroki, M., Abe, K.-i., Dansako, H., Ikeda, M., Wakita, T., Kato, N. (2007). DDX3 DEAD-Box RNA Helicase Is Required for Hepatitis C Virus RNA Replication. J. Virol. 81: 13922-13926 [Abstract] [Full Text]  
  • Masson, C., Bury-Mone, S., Guiot, E., Saez-Cirion, A., Schoevaert-Brossault, D., Brachet-Ducos, C., Delelis, O., Subra, F., Jeanson-Leh, L., Mouscadet, J.-F. (2007). Ku80 Participates in the Targeting of Retroviral Transgenes to the Chromatin of CHO Cells. J. Virol. 81: 7924-7932 [Abstract] [Full Text]  
  • Shun, M.-C., Raghavendra, N. K., Vandegraaff, N., Daigle, J. E., Hughes, S., Kellam, P., Cherepanov, P., Engelman, A. (2007). LEDGF/p75 functions downstream from preintegration complex formation to effect gene-specific HIV-1 integration. Genes Dev. 21: 1767-1778 [Abstract] [Full Text]  
  • Maxwell, P. H., Curcio, M. J. (2007). Host Factors That Control Long Terminal Repeat Retrotransposons in Saccharomyces cerevisiae: Implications for Regulation of Mammalian Retroviruses. Eukaryot Cell 6: 1069-1080 [Full Text]  
  • Ishiguro, A., Ideta, M., Mikoshiba, K., Chen, D. J., Aruga, J. (2007). ZIC2-dependent Transcriptional Regulation Is Mediated by DNA-dependent Protein Kinase, Poly(ADP-ribose) Polymerase, and RNA Helicase A. J. Biol. Chem. 282: 9983-9995 [Abstract] [Full Text]  
  • Stauffer, D., Chang, B., Huang, J., Dunn, A., Thayer, M. (2007). p300/CREB-binding Protein Interacts with ATR and Is Required for the DNA Replication Checkpoint. J. Biol. Chem. 282: 9678-9687 [Abstract] [Full Text]  
  • Ariumi, Y., Trono, D. (2006). Ataxia-Telangiectasia-Mutated (ATM) Protein Can Enhance Human Immunodeficiency Virus Type 1 Replication by Stimulating Rev Function. J. Virol. 80: 2445-2452 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»