Previous Article | Next Article ![]()
Journal of Virology, January 2001, p. 1054-1060, Vol. 75, No. 2
Departments of Medicine and Epidemiology,
School of Veterinary Medicine1 and
Center of Comparative Medicine,2
University of California, Davis, California 95616
Received 23 March 2000/Accepted 24 October 2000
AP-1- and ATF-binding sites are cis-acting
transcriptional elements within the U3 domain of the feline
immunodeficiency virus (FIV) long terminal repeat (LTR) that serve as
targets for cellular activation pathways and may regulate virus
replication. We report that FIV LTR mutant proviruses encoding U3
deletions of the ATF-binding sequence exhibited restricted virus
expression and replication in both feline lymphocytes and macrophages.
In contrast, deletion of the AP-1 site had negligible effects on virus
expression and replication. FIV LTR mutant proviruses encoding
deletions of both the AP-1 and ATF sites or a 72-bp deletion
encompassing the AP-1 site, duplicated C/EBP sites, and ATF sites were
severely restricted for virus expression. These results demonstrate
that deletion of either the ATF-binding site or multiple
cis-acting transcriptional elements attenuates FIV. These
attenuated FIV mutants provide opportunities to characterize the role
of cis-acting elements in virus replication in vivo and to
test LTR mutants as attenuated virus vaccines.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.2.1054-1060.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Construction and In Vitro Characterization of Attenuated Feline
Immunodeficiency Virus Long Terminal Repeat Mutant Viruses
*
Corresponding author. Mailing address: Department of
Medicine and Epidemiology, School of Veterinary Medicine, University of
California, Davis, CA 95616. Phone: (530) 754-8461. Fax: (530) 752-0414. E-mail: eesparger{at}ucdavis.edu.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»