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PubMed · 7889324

Acyclovir-resistant, pathogenic herpesviruses.

D M Coen
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Abstract

In herpes simplex virus, the simplest path to resistance to the drug acyclovir is a mutation that knocks out the enzyme thymidine kinase. Such mutants are highly attenuated in mouse models of viral pathogenesis, but have been reported to be associated with severe disease in immunocompromised patients. This review discusses possible resolution of this paradox.

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AcyclovirAnimalsDrug Resistance, MicrobialHerpes SimplexHumansImmunocompetenceImmunocompromised HostMiceMice, SCIDMutationSimplexvirusThymidine KinaseJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

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D M Coen. 1994. Acyclovir-resistant, pathogenic herpesviruses.. https://doi.org/10.1016/0966-842x(94)90652-1

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Synthesis, DNA binding and antiviral activity of new uracil, xanthine, and pteridine derivatives.

Some new 6-amino-1,3-dimethyl-5-(substituted methylidene)aminouracils were synthesized. Most of them were cyclized with triethyl orthoformate as a one-carbon source to afford 1,3-dime-thyl-6-substituted pteridine derivatives. Certain uracils gave xanthine instead of the expected pteridine derivatives upon using another one-carbon source such as triethyl orthoacetate or triethyl orthobenzoate. The nucleic acid binding assay revealed that some new compounds showed high affinity, chelation, and fragmentation of nucleic acids whether DNA or RNA contrary to acyclovir that has affinity to DNA only. The antiviral activity of these novel compounds showed that compounds 2e and 2f reduced the cytopathogencity of Peste des petits ruminant virus (PPRV) on Vero cell culture by 60 and 50%, respectively.

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