Failure of Guanidine and 2-( -Hydroxybenzyl)benzimidazole to Inhibit Replication of Hepatitis A Virus In vitro

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Abstract
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 2 chemicals effective in combination. Under identical conditions, replication of poliovirus type 1 was inhibited. Tracer experiments with radiolabeled guanidine and D-HBB also furnished no evidence that the 2 antiviral substances were metabolized gradually to inactive derivatives in PLC/PRF/5 cells. Resistance to the action of guanidine and D-HBB appears to be an inherent characteristic of HAV. However, the insensitivity of HAV to these drugs does not exclude the virus from the family of picornaviruses.