Thymidine Kinase Mutations Conferring Acyclovir Resistance in Herpes Simplex Type 1 Recombinant Viruses

Sergerie, Yan; Boivin, Guy

doi:10.1128/aac.00889-06

Cited by 26 publications

(8 citation statements)

References 20 publications

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“…The generation of recombinant mutants following cotransfection of overlapping cosmids and plasmids into permissive cells represents an important improvement (19,52,65,198). This procedure leads to the reconstitution of mutant virus only and circumvents the tedious selection procedure against the parental virus.…”

Section: Laboratory Diagnosis Of Antiviral Drug Resistancementioning

confidence: 99%

Resistance of Herpes Simplex Viruses to Nucleoside Analogues: Mechanisms, Prevalence, and Management

Piret

Boivin

2011

Antimicrob Agents Chemother

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465

406

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Section: Laboratory Diagnosis Of Antiviral Drug Resistancementioning

confidence: 99%

Resistance of Herpes Simplex Viruses to Nucleoside Analogues: Mechanisms, Prevalence, and Management

Piret

Boivin

2011

Antimicrob Agents Chemother

Self Cite

465

406

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“…In this respect, results of genotypic testing must be interpreted by comparison with mutations already assigned to natural polymorphism or confirmed drug resistance in the literature. Mutations with unknown significance in drug resistance must be confirmed by recombinant phenotyping which consists in the introduction of an individual mutation into the genome of a control-sensitive laboratory strain followed by the determination of the resulting drug-susceptibility phenotype (Bestman-Smith and Boivin 2003;Sergerie and Boivin 2006). …”

Section: Herpes Simplex Virus and Varicella-zoster Virus Antiviral Drmentioning

confidence: 99%

Antiviral Drug Resistance in Herpesviruses

Piret

Drouot

Boivin

2014

Handbook of Antimicrobial Resistance

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The discovery of acyclovir (ACV), a nucleoside analogue, more than 30 years ago, represents a milestone in the management of herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections. The modest activity of ACV against human cytomegalovirus (HCMV) has prompted the development of another nucleoside analogue, ganciclovir (GCV), for the management of systemic and organ-specific HCMV diseases. Second-line agents such as the pyrophosphate analogue foscarnet (FOS) and the nucleotide analogue cidofovir (CDV) have been approved subsequently. In contrast to ACV and GCV, the latter drugs do not require an initial phosphorylation step by viral protein kinases to be converted into their active forms. Since the introduction of these antivirals, the emergence of drug-resistant mutants has been constantly reported particularly in severely immunocompromised patients such as bone marrow and solid organ transplant recipients as well as human immunodeficiency virus (HIV)-infected individuals. In this chapter, we review the characteristics of the antiviral agents currently approved for the management of HSV, VZV, and HCMV diseases, the laboratory methods for assessing drug susceptibilities, and the clinical significance of drug-resistant infections and their management.

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“…La sélection du virus recombinant était alors réalisée grâce à un antiviral. Une autre approche consistait à générer des virus recombinants en co-transfectant des cosmides et des plasmides chevauchants dans des cellules permissives [87][88][89]. Plus récemment, la solution permettant de facilement créer des virus recombinants est apparue en détournant la machinerie bactérienne.…”

Section: Utilisation Des Virus Recombinantsunclassified

Herpes simplex virus resistance to antivirals

Burrel¹,

Topalis²,

Boutolleau³

2020

Virologie

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Herpes simplex virus (HSV) infections remain an important cause of morbidity among immunocompromised patients, such as transplant recipients and human immunodeficiency virus [HIV]-infected individuals. Only few antiviral drugs are available to treat HSV infections: (val)acyclovir, foscarnet, and cidofovir. Prophylactic and curative antiviral treatments administered during prolonged periods among patients with altered T-cell immunity may lead to the emergence of HSV resistance to antivirals, contributing to a challenging therapeutic management of viral infection. The persistence of herpetic lesions after 10 days of well-conducted antiviral therapy is suggestive of viral resistance. Resistance to antivirals can be detected using genotypic methods (identifications of antiviral resistance-associated mutations by sequencing genes encoding viral proteins involved in the mechanism of action of antivirals) or phenotypic methods (measure of antiviral drug concentration inhibiting 50% of viral replication in cell culture). The prevalence of HSV resistance to acyclovir is below 1% in immunocompetent individuals, except those with herpetic keratitis for whom prevalence can reach 7%, and varies from 3.5% to 11% in immunocompromised patients. Adverse effects and the absence of eradication of viral latent infection constitute other limits to the use of antiviral drugs. New antiviral compounds undergoing clinical trials and novel potential viral targets seem very promising to enlarge the panel of efficient compound to treat HSV infections.

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Thymidine Kinase Mutations Conferring Acyclovir Resistance in Herpes Simplex Type 1 Recombinant Viruses

Cited by 26 publications

References 20 publications

Resistance of Herpes Simplex Viruses to Nucleoside Analogues: Mechanisms, Prevalence, and Management

Resistance of Herpes Simplex Viruses to Nucleoside Analogues: Mechanisms, Prevalence, and Management

Antiviral Drug Resistance in Herpesviruses

Herpes simplex virus resistance to antivirals

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