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

Piret, Jocelyne; Boivin, Guy

doi:10.1128/aac.00615-10

Cited by 472 publications

(427 citation statements)

References 251 publications

(288 reference statements)

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“…In general, in vitro resistance to acyclovir can be defined by using the concentration of acyclovir that reduces the plaque number by 50% (half maximal inhibitory concentration) and a widely accepted breakpoint value of $2 µg/mL for acyclovir. 12 In addition, half maximal inhibitory concentration values of HSV-1 and -2 with acyclovir are 0.02 to 0.9 and 0.03 to 2.2 µg/mL, respectively. 12 According to these data, our dosing regimen during CRRT appears to be reasonable in attaining the desired serum acyclovir concentrations.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Therapeutic Drug Monitoring in Neonatal HSV Infection on Continuous Renal Replacement Therapy

Funaki¹,

Miyata²,

Shoji³

et al. 2015

Pediatrics

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Optimal acyclovir dosing under continuous renal replacement therapy (CRRT) in neonates is unknown. We monitored serum acyclovir levels and herpes simplex virus 1 (HSV-1) DNA levels in a neonate with disseminated HSV-1 infection and renal failure undergoing CRRT. A full-term, 5-day-old female presented with a 2-day history of lethargy and fever. She developed fulminant hepatitis and was diagnosed with HSV-1 infection by real-time polymerase chain reaction. Acyclovir was initiated at 60 mg/kg/day, which was lowered to 20 mg/kg/day because of development of renal failure. She was placed on continuous hemodialysis. Acyclovir dosing was adjusted according to serum acyclovir levels, and HSV-1 viral load was sequentially monitored. Semiquantification of serum HSV-1 levels was performed by real-time polymerase chain reaction. Acyclovir levels were measured by using liquid chromatography-tandem mass spectrometry. Acyclovir was administered at 20 mg/kg intravenously over 1 hour; peak concentration was 18.9 mg/mL.

show abstract

Section: Discussionmentioning

confidence: 97%

“…12 In addition, half maximal inhibitory concentration values of HSV-1 and -2 with acyclovir are 0.02 to 0.9 and 0.03 to 2.2 µg/mL, respectively. 12 According to these data, our dosing regimen during CRRT appears to be reasonable in attaining the desired serum acyclovir concentrations.…”

Section: Discussionmentioning

confidence: 97%

Therapeutic Drug Monitoring in Neonatal HSV Infection on Continuous Renal Replacement Therapy

Funaki¹,

Miyata²,

Shoji³

et al. 2015

Pediatrics

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show abstract

“…Non-response to foscarnet is also possible, albeit rare. In such cases, IV cidofovir administration (5 mg/kg/week) may be considered [68]. Topical imiquimod is a good alternative in cases where IV treatment is not possible [69][70][71].…”

Section: Cases Of Resistancementioning

confidence: 99%

Genital Herpes

Emre¹,

Akkus²

2017

Fundamentals of Sexually Transmitted Infections

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Genital herpes simplex virus (HSV) infections are among the most commonly seen sexually transmited infections in the world. Genital herpes is a serious health problem because the infection continues through life with remissions and relapses, it causes recurring painful ulcers, and there is no known cure for it. The real prevalence of the genital herpes infection is unknown due to asymptomatic cases. The majority of infected individuals are not aware of the infection due to short duration of symptoms and signs or its asymptomatic nature. The clinical presentation of genital herpes shows certain differences in terms of the primary atack following the irst encounter with the virus and recurrent atacks. There is a strong relationship between HSV-2 positivity and human immunodeiciency virus (HIV). A serious complication of genital herpes in the mother during pregnancy, neonatal herpes, has a mortality risk of 60% if not treated. Antiviral therapy is safe and efective, for both episodic treatment and chronic suppression of HSV. Epidemiology, clinical presentation, laboratory, and treatment options of genital herpes are summarized in this chapter.

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“…Therefore, a deletion, insertion or point mutation, often within a hotspot, of the viral UL23 gene, originates a premature stop codon at one of several different places within the gene (Sasadeusz et al, 1997), resulting in a truncated TK protein, which does not have enzymatic activity (Gilbert et al, 2002;Summers et al, 1975). The TKN strains replicate very slowly because they lack the activity of the viral TK gene, which is required to synthetize deoxythymidine triphosphate for DNA synthesis, and these negative mutants have shown to be impaired in their pathogenicity, establishment of latency and low reactivation efficiency (Piret et al, 2011). In immunocompetent individuals the immune response can rapidly dealt with the viral mutants before they can become clinically apparent (Coen, 1994).…”

Section: Mutations In the Tk Genementioning

confidence: 99%