PMID- 1851861
OWN - NLM
STAT- MEDLINE
DCOM- 19910626
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 65
IP  - 6
DP  - 1991 Jun
TI  - Transactivation of the human immunodeficiency virus promoter by human herpesvirus 
      6 (HHV-6) strains GS and Z-29 in primary human T lymphocytes and identification 
      of transactivating HHV-6(GS) gene fragments.
PG  - 2895-902
AB  - Human herpesvirus 6 (HHV-6) can activate the human immunodeficiency virus (HIV) 
      promoter and accelerate cytopathic effects in HIV-infected human T cells. This 
      study examines the regions of the HIV promoter required for HHV-6 transactivation 
      in a heterogeneous population of primary human T lymphocytes with or without 
      antigenic stimulation. Two different strains of HHV-6, GS and Z29, transactivated 
      the HIV promoter. The GS strain transactivated the promoter in both stimulated 
      and resting T cells, while the Z29 strain increased HIV promoter activity only in 
      stimulated T cells. Three DNA clones containing HHV-6(GS) genomic fragments 
      transactivated the HIV promoter in cotransfected T cells. A 21.4-kb DNA clone, 
      pZVB70, showed the highest transactivating ability, while two other DNA 
      fragments, pZVB10 (6.2 kb) and pZVH14 (8.7 kb), showed lower activity. One of 
      these clones, pZVH14, activated the HIV promoter construct containing a mutation 
      in the NF kappa B site. However, this mutated NF kappa B promoter was not 
      transactivated during HHV-6(GS) infection or after cotransfection with pZVB70 or 
      pZVB10. These data indicate that the NF kappa B sites of the HIV promoter are 
      essential for its transactivation during HHV-6(GS) infection. By increasing HIV 
      promoter activity in primary T lymphocytes, HHV-6 may consequently increase HIV 
      replication, leading to an increase in the cytopathic effect on coinfected human 
      T cells.
FAU - Horvat, R T
AU  - Horvat RT
AD  - Department of Microbiology, University of Kansas, Lawrence 66045.
FAU - Wood, C
AU  - Wood C
FAU - Josephs, S F
AU  - Josephs SF
FAU - Balachandran, N
AU  - Balachandran N
LA  - eng
GR  - AI 24115/AI/NIAID NIH HHS/United States
GR  - AI 24224/AI/NIAID NIH HHS/United States
GR  - AI30355/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (DNA, Viral)
RN  - 0 (NF-kappa B)
RN  - EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
SB  - IM
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chloramphenicol O-Acetyltransferase/metabolism
MH  - Cytopathogenic Effect, Viral
MH  - DNA, Viral/chemistry
MH  - Enhancer Elements, Genetic
MH  - *Gene Expression Regulation, Viral
MH  - HIV/*genetics/growth & development
MH  - HIV Long Terminal Repeat
MH  - Herpesviridae Infections/genetics
MH  - Herpesvirus 6, Human/*genetics
MH  - Humans
MH  - Molecular Sequence Data
MH  - NF-kappa B/genetics
MH  - *Promoter Regions, Genetic
MH  - T-Lymphocytes/*microbiology
MH  - Transfection
MH  - Virus Replication
PMC - PMC240920
EDAT- 1991/06/01 00:00
MHDA- 1991/06/01 00:01
PMCR- 1991/06/01
CRDT- 1991/06/01 00:00
PHST- 1991/06/01 00:00 [pubmed]
PHST- 1991/06/01 00:01 [medline]
PHST- 1991/06/01 00:00 [entrez]
PHST- 1991/06/01 00:00 [pmc-release]
AID - 10.1128/JVI.65.6.2895-2902.1991 [doi]
PST - ppublish
SO  - J Virol. 1991 Jun;65(6):2895-902. doi: 10.1128/JVI.65.6.2895-2902.1991.