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 Google Scholar
Google Scholar
Right arrow Articles by Sroller, V.
Right arrow Articles by Butel, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sroller, V.
Right arrow Articles by Butel, J. S.

 Previous Article  |  Next Article 

Journal of Virology, January 2008, p. 871-879, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01626-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Influence of the Viral Regulatory Region on Tumor Induction by Simian Virus 40 in Hamsters{triangledown}

Vojtech Sroller, Regis A. Vilchez,{dagger} A. Renee Stewart, Connie Wong, and Janet S. Butel*

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030

Received 25 July 2007/ Accepted 24 October 2007

Most of the simian virus 40 (SV40) genome is conserved among isolates, but the noncoding regulatory region and the genomic region encoding the large T-antigen C terminus (T-ag-C) may exhibit considerable variation. We demonstrate here that SV40 isolates differ in their oncogenic potentials in Syrian golden hamsters. Experimental animals were inoculated intraperitoneally with 107 PFU of parental or recombinant SV40 viruses and were observed for 12 months to identify genetic determinants of oncogenicity. The viral regulatory region was found to exert a statistically significant influence on tumor incidence, whereas the T-ag-C played a minor role. Viruses with a single enhancer (1E) were more oncogenic than those with a two-enhancer (2E) structure. Rearrangements in the 1E viral regulatory region were detected in 4 of 60 (6.7%) tumors. Viral loads in tumors varied, with a median of 5.4 SV40 genome copies per cell. Infectious SV40 was rescued from 15 of 37 (40%) cell lines established from tumors. Most hamsters with tumors and many without tumors produced antibodies to T antigen. All viruses displayed similar transforming frequencies in vitro, suggesting that differences in oncogenic potential in vivo were due to host responses to viral infection. This study shows that SV40 strains differ in their biological properties, suggests that SV40 replicates to some level in hamsters, and indicates that the outcome of an SV40 infection may depend on the viral strain present.

* Corresponding author. Mailing address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, Mail Stop BCM385, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-3003. Fax: (713) 798-5019. E-mail: jbutel{at}bcm.edu

{triangledown} Published ahead of print on 31 October 2007.

{dagger} Present address: Global Clinical Development, Infectious Diseases and Dermatology, Schering Plough Research Institute, Kenilworth, NJ 07033.

Journal of Virology, January 2008, p. 871-879, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01626-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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