The CD8 Antiviral Factor (CAF) can suppress HIV-1 transcription from the Long Terminal Repeat (LTR) promoter in the absence of elements upstream of the CATATAA box
1 Currently at the Department of Obstetrics and Gynecology, Magee Women’s Research Institute, University of Pittsburgh, Pittsburgh, USA
2 Pittsburgh Retrovirology Laboratory, Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, 426, Parran Hall, 130, DeSoto Street, Pittsburgh 15261, USA
Virology Journal 2014, 11:130 doi:10.1186/1743-422X-11-130Published: 21 July 2014
The CD8 Antiviral Factor (CAF) suppresses viral transcription from the HIV-1 Long Terminal Repeat (LTR) promoter in a non-cytolytic manner. However, the region on the LTR upon which CAF acts is unknown. Our objective was to determine the region on the LTR upon which CAF acts to suppress HIV-1 transcription.
Serial deletions of the LTR from the 5’ end and inactivating point mutations were made.
Serial deletions of the LTR from the 5’ end indicated the importance of a short ~120 bp segment, containing the 3 SpI sites, CATA box (used by HIV-1 instead of the TATA box) and TAR region, in the suppressive process. Introduction of deletions or inactivating point mutations in the SpI sites or deletion of the TAR region did not abolish CAF-mediated transcriptional suppression. Yet, CAF-mediated transcriptional suppression was still retained in the HIV-1 CATA-TAR segment.
CAF is able to suppress transcription from the LTR lacking all the elements upstream of the CATA box. Our results suggest that the HIV-1 CATA box may be responsible for CAF-mediated suppression of transcription from the HIV-1 LTR.