Influence of cell cycle on the efficiency of transfection with purified human cytomegalovirus DNA

Schneider

Jost

et al. 1989

Immunoblotting with monoclonal as well as polyclonal lamin antibodies revealed that nuclear lamina proteins of human foreskin fibroblasts (HFF) were differentially affected after infection with human cytomegalovirus (HCMV). Lamin A immunoreactivity was progressively lost during the course of the infectious cycle whereas that of lamin C was comparatively stable. This process was not observed in herpes simplex virus-infected HFF. On the other hand, noninfected arrested HFF stimulated by serum to enter S-phase also exhibited loss of lamin A immunoreactivity. Selective in vivo proteolysis of lamin A is suggested as the possible underlying mechanism.

Section: Discussionmentioning

confidence: 99%

Alteration of nuclear lamina protein in human fibroblasts infected with cytomegalovirus (HCMV)

Schneider

Jost

et al. 1989

“…It might further be valid for the cell system described here that butyrate, by elimination of inhibitory host cell functions, allows progression to synthesis of IE and early products. A consecutive second mechanism involved in the butyrate effect is possibly concerned with the release by drug-removal of the infected cell population from Gl-phase into S-phase, a cellular stage known to facilitate production of HCMV progeny [16,21].…”

Section: Summary Cultured Endothelial Cells Are Shown To Be Induced mentioning

confidence: 99%

Induction by sodium butyrate of cytomegalovirus replication in human endothelial cells

Fuhrmann

Franke

et al. 1989

“…As compared with other members of the human herpesvirus group human c:(comegalovirus (HCMV) presents several characteristic properties, e.g. pronounced species specificity, a very long replication cycle (4,5), and a particular dependence on host cell functions (7,20). Yet another property which distinguishes the HCMV host cell system is the sensitivity of virusinduced DNA replication to inhibitors of glycosylation, such as 2-deoxy-Dglucose and tunicamycin (28,39) which are ineffective, on the other hand, on DNA replication in herpes simplex virus (HSV)-infected cells (28).…”

Section: Introductionmentioning

confidence: 99%

Inhibition by monensin of human cytomegalovirus DNA replication

Kaiser

1987

Monensin, at concentrations which depended on the multiplicity of infection, was found to prevent DNA replication of human cytomegalovirus (HCMV) as well as production of viral progeny in human foreskin fibroblasts. The drug did not affect DNA replication of herpes simplex virus. Inhibition of consecutive HCMV DNA synthesis was also observed following delayed addition of the drug within 12-24 hours postinfection, but was fully reversible upon its removal. Viral replication proceeded, however, without impairment in cultures treated with monensin prior to infection. Induction of viral DNA polymerase activity was not impeded by the inhibitor. Analysis of protein- and glycoprotein synthesis revealed that monensin interfered with the production of a number of HCMV-specific polypeptides. Furthermore, evidence was obtained that the drug may hinder intracellular transport of a 135 kd glycopolypeptide.