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.
AuthorsG Siegl, H J Eggers
JournalThe Journal of general virology (J Gen Virol) Vol. 61 (Pt l) Pg. 111-4 (Jul 1982) ISSN: 0022-1317 [Print] ENGLAND
PMID6288846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antigens, Viral
  • Benzimidazoles
  • Guanidines
  • 2-hydroxybenzylbenzimidazole
  • Guanidine
  • Antigens, Viral (analysis)
  • Benzimidazoles (metabolism, pharmacology)
  • Cell Line
  • Guanidine
  • Guanidines (metabolism, pharmacology)
  • Hepatovirus (drug effects, growth & development, immunology)
  • Humans
  • Poliovirus (drug effects)
  • Virus Replication (drug effects)

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