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Acyclovir-resistant, pathogenic herpesviruses

D M Coen1

  • 1Dept of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.

Trends in Microbiology
|December 1, 1994
PubMed
Summary
This summary is machine-generated.

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Herpes simplex virus mutants lacking thymidine kinase are drug-resistant and attenuated in mice. However, these acyclovir-resistant mutants paradoxically cause severe disease in immunocompromised patients.

Area of Science:

  • Virology
  • Immunology
  • Drug Resistance

Background:

  • Herpes simplex virus (HSV) is a common human pathogen.
  • Acyclovir is a primary antiviral medication used to treat HSV infections.
  • Thymidine kinase is a crucial viral enzyme for acyclovir activation.

Purpose of the Study:

  • To explore the paradoxical association between acyclovir-resistant HSV mutants and severe disease in immunocompromised individuals.
  • To reconcile the observed attenuation in mouse models with clinical reports of severe disease.

Main Methods:

  • Review of existing literature on HSV resistance mechanisms.
  • Analysis of viral pathogenesis in different host models (in vitro, mouse models, human patients).
  • Discussion of potential host-pathogen interactions.

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Main Results:

  • HSV mutants with inactivated thymidine kinase exhibit acyclovir resistance.
  • These thymidine kinase-deficient mutants are typically attenuated in immunocompetent hosts and mouse models.
  • Clinical data suggests these mutants can cause severe disease in immunocompromised patients.

Conclusions:

  • The paradox of attenuated yet virulent HSV mutants highlights the complex interplay between viral genetics and host immune status.
  • Understanding this paradox is critical for managing HSV infections in vulnerable populations.
  • Further research is needed to elucidate the precise mechanisms driving severe disease in immunocompromised patients with these resistant strains.