Siegl G, Eggers H J
J Gen Virol. 1982 Jul;61 (Pt l):111-4. doi: 10.1099/0022-1317-61-1-111.
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.
在人肝癌衍生的PLC/PRF/5细胞系中，甲型肝炎病毒（HAV）的复制在存在各种浓度的胍或D-2-（α-羟基苄基）苯并咪唑（D-HBB）时均未受到抑制，并且这两种化学物质联合使用也无效。然而，在相同条件下，1型脊髓灰质炎病毒的复制受到抑制。用放射性标记的胍和D-HBB进行的示踪实验也没有提供证据表明这两种抗病毒物质在PLC/PRF/5细胞中逐渐代谢为无活性的衍生物。因此，得出结论，对胍和D-HBB作用的抗性是HAV的固有特征。然而，HAV对这些药物的不敏感性并不排除该病毒属于小核糖核酸病毒科。
