The polysulfonated compound suramin blocks adsorption and lateral difusion of herpes simplex virus type-1 in vero cells.
Several polysulfonate compounds have been shown to have the potential to inhibit the replication of herpesviruses by blocking binding and penetration of the host cell. We analyzed the actions of the polysulfonate compound suramin on the replication of herpes simplex virus type 1 (HSV-1) and compared them with the actions of heparin. We used the expression of a reporter gene (beta-galactosidase) recombined into the latency-associated transcript region of the 17syn+ strain of HSV-1 to quickly evaluate productive cycle activity and have shown that it can be directly correlated with virus replication under the conditions used. We find that suramin, like heparin, blocks the binding of HSV-1 to the cell membrane. Also, suramin efficiently blocks the cell-to-cell spread of the virus; this effect has not been previously reported. Our control experiments demonstrate that heparin also has some effect on intercellular spread of HSV-1 but to a significantly lesser degree than does suramin. We suggest that suramin and related polysulfonate compounds have potential for developing of antiherpes treatments.
D000818:Animals; D000998:Antiviral Agents / Q000494:pharmacology*; D002522:Chlorocebus aethiops; D004261:DNA Replication; D004279:DNA, Viral / Q000096:biosynthesis; D015870:Gene Expression; D017930:Genes, Reporter; D006493:Heparin / Q000494:pharmacology; D018259:Herpesvirus 1, Human / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D006801:Humans; D008561:Membrane Fusion / Q000187:drug effects* / Q000502:physiology; D013498:Suramin / Q000494:pharmacology*; D013997:Time Factors; D014709:Vero Cells; D010948:Viral Plaque Assay; D014771:Virion / Q000502:physiology; D019065:Virus Assembly; D014779:Virus Replication; D001616:beta-Galactosidase / Q000235:genetics