Genotypic detection of acyclovir-resistant HSV-1: Characterization of 67 ACV-sensitive and 14 ACV-resistant viruses

Frobert, Émilie; Cortay, Jean‐Claude; Ooka, Tadamasa; Najioullah, Fatiha; Thouvenot, D; Lina, Bruno; Morfin, Florence

doi:10.1016/j.antiviral.2008.01.153

Cited by 85 publications

(64 citation statements)

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“…In addition, HSV infections resistant to nucleoside analogues are recognized as a clinical problem among immunocompromised patients (5). The prevalence of resistance is reported to be about 5% among these patients but can reach up to 14 to 30% among patients with allogeneic bone marrow transplants (6). Therefore, there is a need for effective alternatives to nucleoside analogue inhibitors, to provide more-efficient therapy (even after delayed onset) and to counteract resistance.…”

mentioning

confidence: 99%

Pharmacokinetics-Pharmacodynamics of the Helicase-Primase Inhibitor Pritelivir following Treatment of Wild-Type or Pritelivir-Resistant Virus Infection in a Murine Herpes Simplex Virus 1 Infection Model

Biswas

Sukla

Goldner

et al. 2014

Antimicrob Agents Chemother

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mentioning

confidence: 99%

Pharmacokinetics-Pharmacodynamics of the Helicase-Primase Inhibitor Pritelivir following Treatment of Wild-Type or Pritelivir-Resistant Virus Infection in a Murine Herpes Simplex Virus 1 Infection Model

Biswas

Sukla

Goldner

et al. 2014

Antimicrob Agents Chemother

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“…The TaqMan HSV quantitative real-time PCR assay integrating PCR inhibitor detection was performed using an iCycler IQ (Bio-Rad, Marnesla-Coquette, France) as described previously (6). The oligonucleotide primers used for amplification were constructed to detect the HSV-1 and HSV-2 glycoprotein B gene.…”

Section: Methodsmentioning

confidence: 99%

Virological Diagnosis of Herpes Simplex Virus 1 Esophagitis by Quantitative Real-Time PCR Assay

et al. 2012

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Herpes simplex virus 1 (HSV-1) esophagitis diagnosis is routinely based on the endoscopic findings confirmed by histopathological examination of the esophagitis lesions. Virological diagnosis is not systematically performed and restricted to viral culture or to qualitative PCR assay from esophagitis biopsy specimens. The aim of this study was to assess the interest of quantitative real-time PCR assay in HSV-1 esophagitis diagnosis by comparing the results obtained to those of histological examination associated with immunohistochemical staining, which is considered the "gold standard." From 53 esophagitis biopsy specimens, the PCR assay detected HSV-1 in 18 of 19 histologically proven to have herpetic esophagitis and in 9 of 34 that had esophagitis related to other causes, demonstrating sensitivity, specificity, positive predictive value, and negative predictive value of 94.7%, 73%, 66.7%, and 96%, respectively. Interestingly, HSV-1 was not detected in 16 specimens without the histological aspect of esophagitis. The viral loads normalized per g of total extracted DNA in each biopsy specimen detected positive by HSV PCR were then compared and appeared to be significantly higher in histopathologically positive herpetic esophagitis (median ‫؍‬ 2.9 ؋ 10 6 ؎ 1.1 ؋ 10 8 ) than in histopathologically negative herpetic esophagitis (median ‫؍‬ 3.1 ؋ 10 3 ؎ 6.2 ؋ 10 3 ) (P ‫؍‬ 0.0009). Moreover, a receiver operating characteristics analysis revealed that a viral load threshold greater than 2.5 ؋ 10 4 copies would allow an HSV-1 esophagitis diagnosis with a sensitivity and specificity of 83.3% and 100%, respectively. In conclusion, this work demonstrated that HSV quantitative PCR results for paraffin-embedded esophageal tissue was well correlated to histopathological findings for an HSV-1 esophagitis diagnosis and could be diagnostic through viral load assessment when histopathological results are missing or uncertain. Herpes simplex virus 1 (HSV-1) is the second most common infectious etiological cause of esophagitis after Candida albicans (15,18,22). HSV-1 esophagitis is well documented in immunocompromised patients, whereas this clinical entity is rare in immunocompetent patients (2,4,5,9). HSV-1 esophagitis may represent a primary infection in particular in the immunocompetent host but is commonly due to a reactivation of a latent infection in the immunocompromised host (7).Friable mucosa, numerous ulcers, and whitish exudates commonly involving the distal or the midesophagus are classical endoscopic aspects in HSV-1 esophagitis (10,11,14,19). These findings require confirmation by histological examination completed with immunohistochemical staining of the biopsy specimens from the ulcer edges, which still remains the "gold standard" for HSV-1 esophagitis diagnosis (13,14,19). Virological diagnosis has been reported to optimize the diagnostic sensitivity of HSV-1 esophagitis (2,16,19). However, it is not systematically performed and is restricted to viral culture or to qualitative PCR assay from esophageal biopsy speci...

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“…Mutations in the viral TK gene are associated with either polymorphism or drug resistance. The vast majority of mutations unrelated to acyclovir resistance are located outside TK conserved sites (10,19). Table 1 summarizes the HSV-1 UL23 sequencing data for the viral isolates from throat (H723) and skin (H724) lesions that showed differences from published sequences from both human herpesvirus 1 (HHV-1) strain 17 (17) and the HHV-1 strain KOS mutant KG111 (14).…”

Section: Case Reportmentioning

confidence: 99%

“…Based on the published sequence of HHV-1 strain 17 and KOS, the eight UL23 point mutations of our proven acyclovir-sensitive clinical strains are known to be associated with UL23 polymorphism: 23, 36, 240, 251, 267, 268, 286, and 376 (8,10,20). Furthermore, we were able to describe an additional six UL23 point mutations (34, 171, 232, 241, 305, and 351), which are not known to be associated with acyclovir resistance.…”

Section: Vol 46 2008 Case Reports 3163mentioning

confidence: 99%

Thymidine Kinase Sequence Analysis of Herpes Simplex Virus Type 1 Strains Present in Different Compartments in an Atypical Impetiginous Rash on the Lesional Skin of a Burn Patient

et al. 2008

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We report the case of a 23-year-old male burn patient with an unusual herpes simplex virus (HSV) skin manifestation. The clinical symptoms and results of HSV type 1 (HSV-1) UL23 polymorphism analysis from saliva and lesional skin underscores the need for performing molecular analysis of HSV-1 infections in burned patients presenting unusual skin lesions. CASE REPORTAn otherwise healthy, 23-year-old male patient with 32% total body surface area burns was transferred to our burn center. The patient sustained superficial second-degree burns on the face and neck, on both arms, extending from the hand to the upper arms, and on front and back areas of both lower legs and knees. The injury was caused by a workplace-related gas burner explosion.Initially the patient was intubated and a bronchoscopy was performed. There were no signs of an inhalation injury. The wounds were surgically debrided, and a Vaseline gauze dressing was applied. Daily dressing changes were performed.Due to gram-positive bacteria in tracheal secretions, antibiotic treatment with a cephalosporin was administered for 7 days. The patient was extubated on day 7.On postburn day 10, a sudden increase in the patient's temperature to near 39°C was noticed, and a deterioration of his general condition was evident. Pneumonia was excluded by X rays of the chest. At this point we also removed the central line catheter.Twenty-four hours after the onset of fever, the patient developed yellowish seromucus-covered erosions in the burned skin areas. The focal point of the rash was on the arms, the neck, and the underpart of the face ( Fig. 1 and 2). The patient reported merely some light tension on the affected areas but severe pain. Based on the symptoms and the shape of the blisters, we suspected both bacterial and herpes simplex virus type 1 (HSV-1) infection. Swabs of the blister revealed Staphylococcus epidermidis, and molecular analysis for HSV-1, cytomegalovirus (CMV), and varicella-zoster virus (VZV) revealed HSV-1 infection.On admission the patient was immunoglobulin G (IgG) positive for HSV, CMV, and VZV (20 July 2006). No enhanced CMV IgG levels were observed, and no antiherpesvirus IgM was detectable by enzyme-linked immunosorbent assay. A lesional wound swab from skin of the upper arm on postburn day 11 (1 August 2006) revealed the presence of HSV-1 DNA (H724) by a real-time PCR protocol with melting-point analysis for discrimination between HSV-1 and -2 (5). From the same swab, PCR for VZV and CMV DNA was negative. Serology for HSV IgM was negative, and complement fixation revealed an enhanced titer of 160 at 11 days postburn (1 August 2006). On day 12 after the thermal insult (2 August 2006), HSV-1 was isolated from a throat swab (H723) and a throat wash by microculture using monolayers of human foreskin fibroblasts and Vero cells. The HSV-specific cytopathic effects in both cell cultures were confirmed by immunoperoxidase staining of HSV glycoprotein D by an in situ enzyme-linked immunosorbent assay. At the same time, PCR results for CMV from leuko...

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Genotypic detection of acyclovir-resistant HSV-1: Characterization of 67 ACV-sensitive and 14 ACV-resistant viruses

Cited by 85 publications

References 58 publications

Pharmacokinetics-Pharmacodynamics of the Helicase-Primase Inhibitor Pritelivir following Treatment of Wild-Type or Pritelivir-Resistant Virus Infection in a Murine Herpes Simplex Virus 1 Infection Model

Pharmacokinetics-Pharmacodynamics of the Helicase-Primase Inhibitor Pritelivir following Treatment of Wild-Type or Pritelivir-Resistant Virus Infection in a Murine Herpes Simplex Virus 1 Infection Model

Virological Diagnosis of Herpes Simplex Virus 1 Esophagitis by Quantitative Real-Time PCR Assay

Thymidine Kinase Sequence Analysis of Herpes Simplex Virus Type 1 Strains Present in Different Compartments in an Atypical Impetiginous Rash on the Lesional Skin of a Burn Patient

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