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

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.

1976 ◽  
Vol 62 (6) ◽  
pp. 615-622 ◽  
Author(s):  
Giulio Tarro ◽  
Mario Di Gioia ◽  
Roberta Cocchiara ◽  
Riccardo Smeraglia ◽  
Giovan Giacomo Giordano ◽  
...  

Data are reported on the HSV nonstructural antigens detected in GPK and RK cells after infection with the same strain of virus. Both the HSV types 1 and 2 NV antigens consist of more than one component for which the immunized guinea pigs produce distinct antibodies. It was possible to separate by PAGE, HSV-induced markers not only from cells undergoing lytic infection by the virus but also from viable cells from squamous cell carcinoma of the head and neck and the urogenital tract. These fractions were tested with sera from cancer patients, and the percentages of their CF reactivity are reported. The specificity of the antibody to the antigen from the cancer cells was less high than that of the antibody to the antigen from HSV-infected cells. It is suggested that the use of these PAGE separate antigens would eliminate the need for removal of the virion antibody from the cancer sera prior to testing them for the NV-specific antibody.


1987 ◽  
Vol 7 (6) ◽  
pp. 475-483 ◽  
Author(s):  
Nicholas B. LaThangue ◽  
David S. Latchman

A monoclonal antibody defines an antigen, p68, related to hsp70, which is located in nuclei of uninfected exponential cells. Nuclear p68 is released by DNase but not RNase treatment suggesting an association with DNA. Lytic productive infection of confluent quiescent BHK 21 cells with herpes simplex virus type-2 causes p68 to accumulate in nuclei. The effect is specific for HSV-2, and does not occur in HSV-1 infected cells. Maximum nuclear accumulation of p68 requires virus DNA synthesis although a significant accumulation occurs in the absence of such synthesis. It is suggested that the nuclear accumulation of p68 is an aspect of a cellular stress response to lytic infection with HSV-2.


1992 ◽  
Vol 284 (3) ◽  
pp. 667-673 ◽  
Author(s):  
K L Jang ◽  
D S Latchman

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.


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