Transactivation by the Herpes Simplex Virus Virion Protein Vmw65 and Viral Permissivity in a Neuronal Cell Line with Reduced Levels of the Cellular Transcription Factor Oct-1

1993 ◽  
Vol 207 (1) ◽  
pp. 194-196 ◽  
Author(s):  
M.Keith Howard ◽  
Carolina Mailhos ◽  
Carolyn L. Dent ◽  
D.S. Latchman
Keyword(s):  
Transcription Factor ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Line ◽  
Neuronal Cell ◽  
Virion Protein ◽  
Neuronal Cell Line ◽  
Cellular Transcription Factor ◽  
Simplex Virus ◽  
Cellular Transcription

scholarly journals The herpes simplex virus virion protein Vmw65 transcriptionally activates the gene encoding the U4 snRNA but not that encoding the U2 snRNA during lytic infection

1991 ◽  
Vol 275 (2) ◽  
pp. 369-372
Author(s):  
D S Latchman
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Lytic Infection ◽  
Virion Protein ◽  
Gene Encoding ◽  
U2 Snrna ◽  
Cellular Transcription Factor ◽  
Infected Cells ◽  
Simplex Virus ◽  
Cellular Transcription

Although lytic infection with herpes simplex virus (HSV) causes the repression of most host cell biosynthesis, it results in increased transcription of the cellular gene encoding the U4 snRNA, leading to accumulation of this snRNA. In contrast, no increased transcription of the gene encoding the U2 snRNA or accumulation of this RNA is observed in infected cells. These effects are mediated by the HSV virion protein Vmw65, which activates the U4 gene but does not affect the U2 gene. The significance of this difference between the U2 and U4 genes is discussed with regard to the presence in both of these genes of an identical octamer-binding site for the cellular transcription factor Oct-1 which complexes with Vmw65.

Distribution of actin and myosin in a rat neuronal cell line infected with herpes simplex virus

1982 ◽  
Vol 72 (1-2) ◽  
pp. 95-103 ◽  
Author(s):  
M. Winkler ◽  
G. J. Dawson ◽  
T. S. Elizan ◽  
S. Berl
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Line ◽  
Neuronal Cell ◽  
Neuronal Cell Line ◽  
Simplex Virus

scholarly journals The herpes simplex virus immediate-early protein ICP27 stimulates the transcription of cellular Alu repeated sequences by increasing the activity of transcription factor TFIIIC

1992 ◽  
Vol 284 (3) ◽  
pp. 667-673 ◽  
Author(s):  
K L Jang ◽  
D S Latchman
Keyword(s):  
Transcription Factor ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immediate Early ◽  
Cellular Transcription Factor ◽  
Early Protein ◽  
Simplex Virus ◽  
Cellular Transcription ◽  
Increased Activity ◽  
In Cells

Infection with herpes simplex virus (HSV) results in an increase in the transcription of the endogenous Alu repeated sequence by RNA polymerase III. This effect is also observed in uninfected cells stably transformed with a plasmid expressing the HSV immediate-early protein ICP27 or in cells transfected with the gene encoding this protein. Both uninfected cells expressing ICP27 and cells infected with virus producing functional ICP27 display increased activity of the cellular transcription factor TFIIIC when compared with untreated cells. This increase is not observed, however, in cells infected with a mutant strain of virus which does not produce ICP27. Hence ICP27 induces elevated Alu transcription by activating transcription factor TFIIIC, which is the limiting factor for such transcription. This is the first report of increased activity of a cellular transcription factor during HSV infection, when most cellular gene activity is inhibited.

scholarly journals Herpes Simplex Virus Type 1 Latency-Associated Transcripts Suppress Viral Replication and Reduce Immediate-Early Gene mRNA Levels in a Neuronal Cell Line

1998 ◽  
Vol 72 (6) ◽  
pp. 5067-5075 ◽  
Author(s):  
Nurith Mador ◽  
Daniel Goldenberg ◽  
Oren Cohen ◽  
Amos Panet ◽  
Israel Steiner
Keyword(s):  
Herpes Simplex ◽  
Cell Line ◽  
Neuronal Cell ◽  
Mrna Levels ◽  
Neuronal Cell Line ◽  
Simplex Virus ◽  
Negative Mutant ◽  
Gene Mrna ◽  
Hsv 1

ABSTRACT During herpes simplex virus type 1 (HSV-1) latent infection in human dorsal root ganglia, limited viral transcription, which has been linked to HSV-1 reactivation ability, takes place. To study the involvement of this transcription in HSV-1 replication in neuronal cells and consequently in viral latency, we constructed stably transfected neuronal cell lines containing (i) the entire HSV-1 latency transcriptionally active DNA fragment, (ii) the same DNA sequence with deletions of the latency-associated transcript (LAT) promoters, or (iii) the DNA coding sequence of the LAT domain. Replication of HSV-1 or a LAT-negative mutant was markedly repressed in the LAT-expressing cells, a phenomenon mediated by the LATs. To study the mechanism responsible for this effect, we examined LAT influence upon expression of HSV-1 immediate-early (IE) genes ICP0, ICP4, and ICP27, by Northern blot analysis. Following infection of a LAT-expressing neuronal cell line with a LAT-negative mutant, the steady-state levels of all three IE mRNAs were reduced compared to those for control cells. Transient transfections into a neuronal cell line indicated that the LAT suppressive effect upon ICP0 mRNA was mediated directly and was not due to the LAT effect upon the ICP0 promoter. We therefore propose that the LATs may repress viral replication in neuronal cells by reducing IE gene mRNA levels and thus facilitate the establishment of HSV-1 latency in nervous tissue.

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