Failure of guanidine and 2-(alpha-hydroxybenzyl)benzimidazole to inhibit replication of hepatitis A virus in vitro.
Replication of hepatitis A virus (HAV) in the human hepatoma-derived PLC/PRF/5 cell line was neither inhibited in the presence of various concentrations of guanidine or D-2-(alpha-hydroxybenzyl)benzimidazole (D-HBB), nor were the two chemicals effective in combination. Under identical conditions, however, replication of poliovirus type 1 was inhibited. Tracer experiments with radiolabelled guanidine and D-HBB also furnished no evidence that the two antiviral substances were metabolized gradually to inactive derivatives in PLC/PRF/5 cells. Therefore, it is concluded that resistance to the action of guanidine and D-HBB is an inherent characteristic of HAV. However, the insensitivity of HAV to these drugs does not exclude the virus from the family of picornaviruses.
D000956:Antigens, Viral / Q000032:analysis; D001562:Benzimidazoles / Q000378:metabolism / Q000494:pharmacology*; D002460:Cell Line; D019791:Guanidine; D006146:Guanidines / Q000378:metabolism / Q000494:pharmacology*; D006507:Hepatovirus / Q000187:drug effects* / Q000254:growth & development / Q000276:immunology; D006801:Humans; D017955:Poliovirus / Q000187:drug effects; D014779:Virus Replication / Q000187:drug effects
D000956:Antigens, Viral; D001562:Benzimidazoles; D006146:Guanidines; C020359:2-hydroxybenzylbenzimidazole; D019791:Guanidine