Suppression of generation and replication of acyclovir-resistant herpes simplex virus by a sensitive virus.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Additional Information
    • Source:
      Publisher: Wiley-Liss Country of Publication: United States NLM ID: 7705876 Publication Model: Print Cited Medium: Print ISSN: 0146-6615 (Print) Linking ISSN: 01466615 NLM ISO Abbreviation: J Med Virol Subsets: MEDLINE
    • Publication Information:
      Publication: New York Ny : Wiley-Liss
      Original Publication: New York, Liss.
    • Subject Terms:
      Drug Resistance, Viral*; Acyclovir/*pharmacology ; Antiviral Agents/*pharmacology ; Herpesvirus 1, Human/*drug effects ; Idoxuridine/*analogs & derivatives ; Virus Replication/*drug effects; Animals ; Chlorocebus aethiops ; Female ; Herpes Simplex/virology ; Herpesvirus 1, Human/metabolism ; Herpesvirus 1, Human/physiology ; Humans ; Idoxuridine/pharmacology ; Mice ; Mice, Inbred BALB C ; Phosphonoacetic Acid/pharmacology ; Serial Passage ; Thymidine Kinase/deficiency ; Thymidine Kinase/metabolism ; Vero Cells ; Viral Plaque Assay
    • Abstract:
      The role of acyclovir-sensitive herpes simplex virus (HSV) was analyzed in the process of its replacement by a resistant virus in vitro and in vivo in the aspect of acyclovir therapy. The mode of replacement of acyclovir-sensitive HSV with acyclovir-resistant HSV was examined by the passages of acyclovir-sensitive wild type HSV in Vero cells under acyclovir-treatment. The development of resistance was monitored more adequately by counting the number of acyclovir-resistant viruses in 10,000 plaque forming units than by the conventional susceptibility assay. The resistance increased with the proportion of thymidine kinase-deficient (TK(-)) viruses, when the susceptibilities of acyclovir-treated HSV population to 5'-iodo-2'deoxyuridine and phosphonoacetic acid were examined. The increased resistance was due to the increased proportion of acyclovir-resistant virus but not intermediately resistant virus. Infection with mixtures of TK(-) and acyclovir-sensitive strains rendered TK(-) sensitive to acyclovir, and virus yields were reduced to the levels of acyclovir-sensitive virus in Vero cells. Their yield reduction depended on the proportion of acyclovir-sensitive viruses and induction of TK activity. This reduction in virus yields of the mixture of TK(-) and acyclovir-sensitive strains was confirmed by acyclovir treatment in the skin of mice with cutaneous infection. Acyclovir treatment combined with superinfection of acyclovir-sensitive virus delayed the development of herpetic skin lesions due to acyclovir-resistant virus and reduced virus yields in the infected skin. Acyclovir-sensitive virus plays an important role in suppressing the generation and replication of acyclovir-resistant virus during acyclovir therapy.
      (Copyright 2004 Wiley-Liss, Inc.)
    • Accession Number:
      0 (Antiviral Agents)
      14259-58-6 (5'-deoxy-5'-iodouridine)
      EC 2.7.1.21 (Thymidine Kinase)
      LGP81V5245 (Idoxuridine)
      N919E46723 (Phosphonoacetic Acid)
      X4HES1O11F (Acyclovir)
    • Publication Date:
      Date Created: 20031125 Date Completed: 20040212 Latest Revision: 20191210
    • Publication Date:
      20231215
    • Accession Number:
      10.1002/jmv.10562
    • Accession Number:
      14635018