Herpes simplex virus type 2 and pseudorabies virus associated growth factors and their role in the latency in vitro
Jazyk angličtina Země Švýcarsko Médium print
Typ dokumentu časopisecké články
PubMed
1284865
Knihovny.cz E-zdroje
- MeSH
- aktivace viru MeSH
- azacytidin farmakologie MeSH
- embryo savčí MeSH
- fenotyp MeSH
- glykoproteiny izolace a purifikace farmakologie fyziologie MeSH
- HeLa buňky účinky léků MeSH
- lidé MeSH
- monoklonální protilátky imunologie MeSH
- myši MeSH
- nádorová transformace buněk účinky léků MeSH
- nádorové buňky kultivované MeSH
- neutralizační testy MeSH
- prasečí herpesvirus 1 fyziologie MeSH
- proteiny virového obalu genetika imunologie MeSH
- protilátky virové imunologie MeSH
- růstové látky izolace a purifikace farmakologie fyziologie MeSH
- Simplexvirus imunologie fyziologie MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- azacytidin MeSH
- glycoprotein B, herpes simplex virus type 2 MeSH Prohlížeč
- glykoproteiny MeSH
- monoklonální protilátky MeSH
- proteiny virového obalu MeSH
- protilátky virové MeSH
- růstové látky MeSH
A putative herpes simplex virus type 2 (HSV-2) growth factor (HSGF-2) was detected in a crude extract from virus infected mouse embryo cells. This factor, similar to previously described pseudorabies virus (PRV) associated growth factor (PRGF) was shown to have ability to morphologically transform non-transformed cells and to repress the transformed phenotype of transformed cells. Both activities could be neutralized with two, out of seven monoclonal antibodies directed against glycoprotein B of HSV-2. Both PRGF and HSGF-2 were detected in human embryo lung cells latently infected with PRV or HSV-2 either at 41 degrees C, or in the presence of phosphonoacetic acid. Human alpha-2 interferon, when present in medium of latently infected cells enhanced the production of both HSGF and PRGF. On the contrary, when latently infected cells were treated with 5-azacytidine the synthesis of both PRGF and HSGF-2 was completely blocked and the virus reactivated from latency replicated to higher titers than in non-treated cells. The role of PRGF and HSGF-2 in the establishment, maintenance and reactivation of latency, as well as in cellular transformation is discussed.