PMID- 21159864
OWN - NLM
STAT- MEDLINE
DCOM- 20110404
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 85
IP  - 5
DP  - 2011 Mar
TI  - Functional characterization of Kaposi's sarcoma-associated herpesvirus open 
      reading frame K8 by bacterial artificial chromosome-based mutagenesis.
PG  - 1943-57
LID - 10.1128/JVI.02060-10 [doi]
AB  - The open reading frame K8 of Kaposi's sarcoma-associated herpesvirus (KSHV) 
      encodes a basic leucine zipper (bZip) protein that binds to the origin of viral 
      DNA replication and is an integral component of viral lytic DNA replication 
      complex. Moreover, K8 physically interacts with replication and transcription 
      activator (RTA) and represses its transactivation activity on several viral 
      promoters. To investigate the role of this protein in viral life cycle, we 
      constructed two K8-null recombinant mutant viruses (BAC-DeltaK8 and BAC-stopK8) by 
      using a bacterial artificial chromosome (BAC) system. Latent viral infection can 
      be reconstituted in 293T and BJAB cells with wild-type and the K8-null 
      recombinant viruses by introducing the cloned viral genomes into the cells. When 
      the cells carrying these viruses were induced with 
      12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate, no significant 
      difference was seen in overall viral gene expression between wild-type and 
      K8-null viruses, with lytic DNA replication still active in the latter. However, 
      293T cells harboring K8-null mutant viruses, either BAC-DeltaK8 or BAC-stopK8, 
      displayed lower copy numbers of latent KSHV genome in comparison with wild-type 
      viruses. Furthermore, although K8 deficiency appeared to not affect infectivity 
      when K8-null viruses were used to infect 293T, primary human microvascular dermal 
      endothelial and human foreskin fibroblast cells, they exhibited much lower viral 
      genome copy numbers in all types of cell compared to wild-type viruses. Taken 
      together, these data suggest a possible role of K8 in abortive lytic DNA 
      replication occurring in early stages of de novo infection or in the maintenance 
      of latent viral genomes.
FAU - Wang, Yan
AU  - Wang Y
AD  - Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, 
      USA.
FAU - Sathish, Narayanan
AU  - Sathish N
FAU - Hollow, Charles
AU  - Hollow C
FAU - Yuan, Yan
AU  - Yuan Y
LA  - eng
GR  - R01CA86839/CA/NCI NIH HHS/United States
GR  - R01 CA086839/CA/NCI NIH HHS/United States
GR  - R01 AI052789-10/AI/NIAID NIH HHS/United States
GR  - R01 CA086839-10/CA/NCI NIH HHS/United States
GR  - R01 AI052789/AI/NIAID NIH HHS/United States
GR  - R01AI052789/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20101215
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Basic-Leucine Zipper Transcription Factors)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Base Sequence
MH  - Basic-Leucine Zipper Transcription Factors/genetics/*metabolism
MH  - Cell Line
MH  - Chromosomes, Artificial, Bacterial/*genetics
MH  - Gene Expression Regulation, Viral
MH  - Herpesviridae Infections/*virology
MH  - Herpesvirus 8, Human/*genetics/physiology
MH  - Humans
MH  - Molecular Sequence Data
MH  - *Mutagenesis
MH  - *Open Reading Frames
MH  - Viral Proteins/genetics/*metabolism
MH  - Virus Replication
PMC - PMC3067771
EDAT- 2010/12/17 06:00
MHDA- 2011/04/05 06:00
PMCR- 2011/09/01
CRDT- 2010/12/17 06:00
PHST- 2010/12/17 06:00 [entrez]
PHST- 2010/12/17 06:00 [pubmed]
PHST- 2011/04/05 06:00 [medline]
PHST- 2011/09/01 00:00 [pmc-release]
AID - JVI.02060-10 [pii]
AID - 2060-10 [pii]
AID - 10.1128/JVI.02060-10 [doi]
PST - ppublish
SO  - J Virol. 2011 Mar;85(5):1943-57. doi: 10.1128/JVI.02060-10. Epub 2010 Dec 15.