The synthesis of the major DNA-binding protein (ICP8) in cells infected with the strain HSZP or KOS of herpes simplex virus type 1
Jazyk angličtina Země Švýcarsko Médium print
Typ dokumentu srovnávací studie, časopisecké články
PubMed
1683115
Knihovny.cz E-zdroje
- MeSH
- DNA vazebné proteiny MeSH
- DNA virů metabolismus MeSH
- druhová specificita MeSH
- fibroblasty MeSH
- jaderná matrix metabolismus MeSH
- králíci MeSH
- kultivované buňky MeSH
- kyselina fosfonoctová farmakologie MeSH
- posttranslační úpravy proteinů účinky léků MeSH
- regulace exprese virových genů účinky léků MeSH
- replikace DNA MeSH
- Simplexvirus klasifikace účinky léků metabolismus fyziologie MeSH
- Vero buňky MeSH
- virové proteiny biosyntéza MeSH
- zvířata MeSH
- Check Tag
- králíci MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- srovnávací studie MeSH
- Názvy látek
- DNA vazebné proteiny MeSH
- DNA virů MeSH
- ICP8 protein, Simplexvirus MeSH Prohlížeč
- kyselina fosfonoctová MeSH
- virové proteiny MeSH
Synthesis of the major DNA-binding protein (ICP8) was investigated in primary rabbit kidney (RK) and Vero cells infected with the syncytial (syn) strain HSZP or with the non-syn strain KOS of herpes simplex virus type 1 (HSV-1). Results showed the following: 1. In contrast to strain KOS, the rate of viral polypeptide synthesis was accelerated in Vero cells infected with strain HSZP. The ICP8 could be detected in the nuclei of cells by one hour post-infection (hr p. i.) where it became associated with the viral DNA (DNase sensitive form). Later on (7 hr p.i.), the synthesis of viral polypeptides decreased and no further translocation of ICP8 from the cytoplasm into the nucleus was observed. 2. Strain HSZP was approx. three times more resistant to the action of phosphonoacetic acid (PAA) than strain KOS. In order to block the synthesis of HSZP gamma-2 polypeptides, a concentration of 600 micrograms PAA/ml had to be used. Under this condition, the HSZP ICP8 was translocated into the cell nucleus at later interval only (7 hr p.i.), and it was still possible to release this polypeptide from the nucleus by DNase treatment. The failure of the HSZP ICP8 to associate with the nuclear matrix (DNase resistant form) of infected cells in the absence of viral DNA replication may reflect its predominant affinity for the viral DNA which, in turn, may be responsible for the observed accelerated synthesis of the HSZP polypeptides in infected Vero cells. 3. In primary RK cells infected with strain HSZP the ICP8 did not translocate into the cell nucleus. Therefore, no gamma-2 polypeptides were synthesized.