Failure of guanidine and 2-(alpha-hydroxybenzyl)benzimidazole to inhibit replication of hepatitis A virus in vitro.

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 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.

• Authors: G Siegl, H J Eggers
• Journal: The Journal of general virology (J Gen Virol) Vol. 61 (Pt l) Pg. 111-4 (Jul 1982) ISSN: 0022-1317 [Print] England
• PMID: 6288846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antigens, Viral
• Benzimidazoles
• Guanidines
• 2-hydroxybenzylbenzimidazole
• Guanidine

Topics

• 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)