Growth Inhibition of Herpes simplex Virus-Type 1 in Calphostin C-Treated Astrocytes

Abstract

The aim was to evaluate the effects of calphostin C (CC), a protein kinase C inhibitor, on lytic herpes simplex virus-type 1 infection of cultured rat astrocytes. At 24 h postinjection, the cell culture receiving CC treatment at 50 nM concentration showed decreased cell detachment and retraction versus untreated infected controls; likewise, the infective virus yield was significantly lower in a dose-dependent manner. In contrast, image analysis failed to disclose differences in viral antigen immunolabeling at low drug concentrations, thus suggesting that CC-induced inhibition of cytopathic effects and infectivity takes place through mechanisms not involving viral protein synthesis. Given the low dose required and the apparent lack of cytotoxic effects, present findings encourage additional studies on CC antiviral potential in the whole organism.

Herpes simplex virus-type 2 infectivity and agents that block gap junctional intercellular communication

“…Yura et al (1993Yura et al ( , 1997 found that genistein, a tyrosine kinase inhibitor, reduced plaque forming ability in Vero cells and prevented phosphorylation of viral polypeptides, particularly ICP 6, 19, and 26 which were necessary for HSV-1 replication. Calphostin C, a protein kinase C inhibitor, reduced HSV-1 infectivity and virus yield in astrocytes without causing an alteration in viral protein synthesis (Castagnino et al, 1995). Constantinescu et al (1991) found that protein kinase C inhibitors reduced infectivity of enveloped, but not non-enveloped viruses, presumably exerting their effects at the level of viral entry.…”