Transcriptional activation is not responsible for increased levels of autonomously expressed simian virus 40 T-antigen in herpes simplex virus-infected cells

Virus Genes ◽  
1989 ◽  
Vol 2 (3) ◽  
pp. 253-267
Author(s):  
Edward D. Blair ◽  
B. Wendy Snowden ◽  
Edward K. Wagner
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Transcriptional Activation ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Infected Cells ◽  
Simplex Virus

scholarly journals Variation in intracellular P1P4-bis(5′-adenosyl) tetraphosphate (Ap4A) in virus-infected cells

1990 ◽  
Vol 268 (3) ◽  
pp. 791-793 ◽  
Author(s):  
D J Johnston ◽  
C A Hart ◽  
A G McLennan
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Infection ◽  
Simian Virus 40 ◽  
Fold Increase ◽  
Vero Cells ◽  
Simian Virus ◽  
Infected Cells ◽  
Simplex Virus

The effect of virus infection on the intracellular concentration of the proposed stress alarmone P1P4-bis(5′-adenosyl) tetraphosphate (Ap4A) has been examined in Vero cells. Compared with exposure to 0.8 mM-Cd2+, which causes a 30-fold increase in Ap4A, infection with simian virus 40 and poliovirus causes only a 2-fold increase, whereas herpes simplex virus type 1 results in a decrease in Ap4A during the course of the infection.

scholarly journals Methylation of single sites within the herpes simplex virus tk coding region and the simian virus 40 T-antigen intron causes gene inactivation.

1994 ◽  
Vol 14 (3) ◽  
pp. 2004-2010 ◽  
Author(s):  
A Graessmann ◽  
G Sandberg ◽  
E Guhl ◽  
M Graessmann
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Synthesis ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Coding Region ◽  
Simplex Virus

In order to determine whether partial methylation of the herpes simplex virus (HSV) tk gene prevents tk gene expression, the HSV tk gene was cloned as single-stranded DNA. By in vitro second-strand DNA synthesis, specific HSV tk gene segments were methylated, and the hemimethylated DNA molecules were microinjected into thymidine kinase-negative rat2 cells. Conversion of the hemimethylated DNA into symmetrical methylated DNA and integration into the host genome occurred early after gene transfer, before the cells entered into the S phase. HSV tk gene expression was inhibited either by promoter methylation or by methylation of the coding region. Using the HindIII-SphI HSV tk DNA fragment as a primer for in vitro DNA synthesis, all cytosine residues within the coding region, from +499 to +1309, were selectively methylated. This specific methylation pattern caused inactivation of the HSV tk gene, while methylation of the cytosine residues within the nucleotide sequence from +811 to +1309 had no effect on HSV tk gene activity. We also methylated single HpaII sites within the HSV tk gene using a specific methylated primer for in vitro DNA synthesis. We found that of the 16 HSV tk HpaII sites, methylation of 6 single sites caused HSV tk inactivation. All six of these "methylation-sensitive" sites are within the coding region, including the HpaII-6 site, which is 571 bp downstream from the transcription start site. The sites HpaII-7 to HpaII-16 were all methylation insensitive. We further inserted separately the methylation-sensitive HSV tk HpaII-6 site and the methylation-insensitive HpaII-13 site as DNA segments (32-mer) into the intron region of the simian virus 40 T antigen (TaqI site). Methylation of these HpaII sites caused inhibition of simian virus 40 T-antigen synthesis.

scholarly journals Successful Retroviral Gene Transfer of Simian Virus 40 T Antigen and Herpes Simplex Virus-Thymidine Kinase into Human Hepatocytes

2001 ◽  
Vol 10 (4-5) ◽  
pp. 377-381 ◽  
Author(s):  
Naoya Kobayashi ◽  
Hirofumi Noguchi ◽  
Karen A. Westerman ◽  
Takamasa Watanabe ◽  
Toshihisa Matsumura ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Gene Transfer ◽  
Thymidine Kinase ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Human Hepatocytes ◽  
Retroviral Gene Transfer ◽  
Simplex Virus

scholarly journals Gonadal tumors of mice double transgenic for inhibin-alpha promoter-driven simian virus 40 T-antigen and herpes simplex virus thymidine kinase are sensitive to ganciclovir treatment

2001 ◽  
Vol 170 (1) ◽  
pp. 79-90 ◽  
Author(s):  
MK Mikola ◽  
NA Rahman ◽  
TH Paukku ◽  
PM Ahtiainen ◽  
TE Vaskivuo ◽  
...  
Keyword(s):  
Body Weight ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Somatic Cell ◽  
Thymidine Kinase ◽  
Fusion Gene ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Simplex Virus

We have previously produced transgenic (TG) mice expressing the mouse inhibin alpha-subunit promoter/Simian virus 40 T-antigen (Inhalpha/Tag) fusion gene. The mice develop gonadal somatic cell tumors at the age of 5-7 months; the ovarian tumors originate from granulosa cells, and those of the testes from Leydig cells. In the present study another TG mouse line was produced, expressing under the same inh-alpha promoter the herpes simplex virus thymidine kinase gene (Inhalpha/TK). Crossbreeding of the two TG mouse lines resulted in double TG mice (Inhalpha/TK-Inhalpha/Tag), which also developed gonadal tumors. The single (Inhalpha/Tag) and double TG (Inhalpha/TK-Inhalpha/Tag) mice, both bearing gonadal tumors, were treated at the age of 5.5-6.5 months with ganciclovir (GCV, 150 mg/kg body weight twice daily i.p.) for 14 days, or with aciclovir (ACV, 300-400 mg/kg body weight per day perorally) for 2 months. During GCV treatment, the total gonadal volume including the tumor, decreased in double TG mice by an average of 40% (P<0.05), while in single TG mice, there was a concomitant increase of 60% in gonadal size (P<0.05). GCV was also found to increase apoptosis in gonads of the double TG mice. Peroral treatment with ACV was less effective, it did not reduce significantly the gonadal volume. We also analyzed the in vitro efficacy of ACV and GCV treatments in transiently HSV-TK-transfected KK-1 murine granulosa tumor cells, originating from a single-positive Inhalpha/Tag mouse. GCV proved to be more effective and more specific than ACV in action. These results prove the principle that targeted expression of the HSV-TK gene in gonadal somatic cell tumors is potentially useful for tumor ablation by antiherpes treatment. The findings provide a lead for further development of somatic gene therapy for gonadal tumors.

scholarly journals Structure of Simian Virus 40 DNA Replicated by Herpes Simplex Virus Type 1

Virology ◽  
2000 ◽  
Vol 276 (2) ◽  
pp. 445-454 ◽  
Author(s):  
Johannes Blümel ◽  
Sascha Gräper ◽  
Bertfried Matz
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Simplex Virus

Herpes simplex virus induces the replication of foreign DNA

1988 ◽  
Vol 8 (8) ◽  
pp. 3272-3281
Author(s):  
R M Danovich ◽  
N Frenkel
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Polymerase ◽  
Replication Origin ◽  
Simian Virus 40 ◽  
T Antigen ◽  
Rabbit Skin ◽  
Skin Cells ◽  
Foreign Dna ◽  
Simplex Virus

Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.

scholarly journals Herpes simplex virus induces the replication of foreign DNA.

1988 ◽  
Vol 8 (8) ◽  
pp. 3272-3281 ◽  
Author(s):  
R M Danovich ◽  
N Frenkel
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Dna Polymerase ◽  
Replication Origin ◽  
Simian Virus 40 ◽  
T Antigen ◽  
Rabbit Skin ◽  
Skin Cells ◽  
Foreign Dna ◽  
Simplex Virus

Plasmids containing the simian virus 40 (SV40) DNA replication origin and the large T gene are replicated efficiently in Vero monkey cells but not in rabbit skin cells. Efficient replication of the plasmids was observed in rabbit skin cells infected with herpes simplex virus type 1 (HSV-1) and HSV-2. The HSV-induced replication required the large T antigen and the SV40 replication origin. However, it produced concatemeric molecules resembling replicative intermediates of HSV DNA and was sensitive to phosphonoacetate at concentrations known to inhibit the HSV DNA polymerase. Therefore, it involved the HSV DNA polymerase itself or a viral gene product(s) which was expressed following the replication of HSV DNA. Analyses of test plasmids lacking SV40 or HSV DNA sequences showed that, under some conditions, HSV also induced low-level replication of test plasmids containing no known eucaryotic replication origins. Together, these results show that HSV induces a DNA replicative activity which amplifies foreign DNA. The relevance of these findings to the putative transforming potential of HSV is discussed.

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