PMID- 8178493
OWN - NLM
STAT- MEDLINE
DCOM- 19940608
LR  - 20220408
IS  - 0042-6822 (Print)
IS  - 0042-6822 (Linking)
VI  - 201
IP  - 1
DP  - 1994 May 15
TI  - Transcriptional activation of minimal HIV-1 promoter by ORF-1 protein expressed 
      from the SalI-L fragment of human herpesvirus 6.
PG  - 95-106
AB  - The SalI-L fragment of human herpesvirus 6 (HHV-6) strain U1102 transformed 
      rodent cells and transactivated the HIV-1 LTR 10- to 15-fold in both monkey 
      fibroblasts and human T-lymphocytes. In this report, the SalI-L transactivator of 
      the HIV-1 LTR was localized to ORF-1 which codes for a protein of 357 amino 
      acids. To determine if ORF-1 required functional Sp1 binding sites or the TATA 
      box element of HIV-1 LTR for transactivation, 5'-deletion mutants of the HIV-1 
      LTR were employed. Plasmids pBS/SalI-L, pBS/SalI-L-SH, and pC6/ORF-1(S), a 
      mammalian expression vector containing ORF-1, all transactivated a deletion 
      mutant of HIV-1 LTR lacking functional Sp1 binding sites (CD-54). These studies 
      demonstrate that transactivation occurred in the absence of Sp1 binding sites and 
      required only a minimal HIV-1 promoter which contains the TATA box element. The 
      specificity of the SalI-L transactivator for HIV-1 LTR was demonstrated by its 
      inability to transactivate the human papillomavirus type 16 or 18 early 
      promoters. The ORF-1 gene was cloned into and expressed from the pET17b bacterial 
      expression vector. Purified ORF-1 protein was obtained by ammonium sulfate 
      precipitation, Mono-S chromatography, and anti-T7. Tag immunoaffinity 
      chromatography. Transactivation of the HIV-1 LTR by ORF-1 protein was 
      demonstrated by electroporation studies in vivo and by transcription studies in 
      vitro. To substantiate the putative biological role of ORF-1, pBS/SalI-L, 
      pBS/SalI-L-SH, and pC6/ORF-1 all reactivated tat-defective HIV-1 provirus from 
      latently infected cells expressing CD4. Thus, the data presented suggest that 
      HHV-6 infection could have a cofactor role in the progression of AIDS.
FAU - Kashanchi, F
AU  - Kashanchi F
AD  - Department of Microbiology and Immunology, Georgetown University Medical Center, 
      Washington, DC 20007.
FAU - Thompson, J
AU  - Thompson J
FAU - Sadaie, M R
AU  - Sadaie MR
FAU - Doniger, J
AU  - Doniger J
FAU - Duvall, J
AU  - Duvall J
FAU - Brady, J N
AU  - Brady JN
FAU - Rosenthal, L J
AU  - Rosenthal LJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Virology
JT  - Virology
JID - 0110674
RN  - 0 (HIV Core Protein p24)
RN  - 0 (ORF-1 protein, Human herpesvirus 6)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Trans-Activators)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Cell Line
MH  - Gene Deletion
MH  - Genes, Viral/genetics
MH  - HIV Core Protein p24/analysis
MH  - HIV Long Terminal Repeat/*genetics
MH  - HIV-1/*genetics/physiology
MH  - Herpesvirus 6, Human/*genetics
MH  - Humans
MH  - Molecular Sequence Data
MH  - *Oncogenes
MH  - Open Reading Frames/genetics
MH  - Promoter Regions, Genetic/genetics
MH  - Recombinant Fusion Proteins/analysis/genetics
MH  - Sequence Alignment
MH  - Sp1 Transcription Factor/genetics
MH  - Trans-Activators/analysis/chemistry/*genetics
MH  - Transcriptional Activation/*genetics
MH  - Transfection
MH  - Tumor Cells, Cultured
MH  - Viral Proteins/analysis/chemistry/*genetics
MH  - Virus Activation
MH  - Virus Latency
EDAT- 1994/05/15 00:00
MHDA- 1994/05/15 00:01
CRDT- 1994/05/15 00:00
PHST- 1994/05/15 00:00 [pubmed]
PHST- 1994/05/15 00:01 [medline]
PHST- 1994/05/15 00:00 [entrez]
AID - S0042-6822(84)71269-4 [pii]
AID - 10.1006/viro.1994.1269 [doi]
PST - ppublish
SO  - Virology. 1994 May 15;201(1):95-106. doi: 10.1006/viro.1994.1269.