Discrimination of Herpes Simplex Virus Type 2 Strains by Nucleotide Sequence Variations

Kaneko, Hisatoshi; Kawana, Takashi; Ishioka, Ken; Fukushima, Eiko; Suzutani, Tatsuo

doi:10.1128/jcm.01615-07

Cited by 9 publications

(11 citation statements)

References 13 publications

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“…While TK, POL, and gD genes were found highly conserved among HSV-2 isolates, gB and gG genes offered a noticeable number of variability hot spots which made these genes suitable tools for the differentiation of viral strains. This conclusion is supported by the previous use of the variability of these genes for classification of HSV-2 isolates [Terhune et al, 1998;Norberg et al, 2007;Kaneko, 2008;Schmidt-Chanasit et al, 2010;]. Moreover, many of the genetic polymorphisms of gB and gD described in the present study have been already reported in previous publications [Terhune et al, 1998;Norberg et al, 2007;Kaneko, 2008].…”

Section: Discussionsupporting

confidence: 91%

Impact of HIV‐1 infection on herpes simplex virus type 2 genetic variability among co‐infected individuals

Abrão¹,

Burrel

Désiré³

et al. 2014

Journal of Medical Virology

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Herpes simplex virus type 2 (HSV-2) is the most common cause of genital ulcer disease worldwide. While the contribution of HSV-2 to acquisition and course of human immunodeficiency virus (HIV) infection has been well described, less attention has been paid to the impact of HIV infection on the variability and the pathophysiology of HSV-2 infection. The goal of the present study was to characterize genotypically and phenotypically HSV-2 strains isolated from 12 patients infected by HIV-1 and from 12 HIV-negative patients. Replication capacity analyses were carried out in Vero cells and full-length nucleotide sequences were determined for glycoproteins B (gB), D (gD), G (gG), thymidine kinase (TK), and DNA polymerase (POL) HSV-2 genes. Sequence alignments and phylogenetic trees were performed. No significant differences were found in terms of replication capacity. The interstrain nucleotide identities of the 3 glycoprotein genes (gB, gC, and gG) ranged from 99.5% to 100% among the 24 HSV-2 strains. The phylogenetic analysis showed no clustering of HSV-2 strains when correlating to the HIV status of the patients. A lower variability was observed for the functional proteins TK and DNA polymerase (98.9% to 100% identity). Genetic analysis of TK evidenced mutations related to acyclovir-resistance in two HSV-2 strains. No specific differences regarding replication capacity and gene sequence were found when comparing HSV-2 strains isolated from patients infected with HIV-1 and HIV-negative patients, suggesting that the virological properties of HSV-2 infection are not influenced by HIV-1 infection among co-infected patients.

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Section: Discussionsupporting

confidence: 91%

Impact of HIV‐1 infection on herpes simplex virus type 2 genetic variability among co‐infected individuals

Abrão¹,

Burrel

Désiré³

et al. 2014

Journal of Medical Virology

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“…This variation is higher than the maximal 0.4% variance noted by Norberg et al among 47 strains sequenced in the US4, US7, and US8 regions. Kaneko et al noted that many HSV-2 genes were completely invariant in Japan (e.g., UL4, UL5, UL12, and 9 other genes) (15). The low dN/dS ratio observed for UL23 is consistent with active selection to preserve certain amino acid sequences despite the apparent tolerance for amino acid changes in many locations.…”

Section: Discussionmentioning

confidence: 70%

“…In our data set, sequences from Peru were admixed with African sequences in all major branches of the UL23 neighbor-joining tree. Kaneko et al sequenced 36 HSV-2 genes from 36 subjects in Japan (15). They analyzed UL3, US1, and US4, their most divergent loci, as trees and noted that they had differing topologies.…”

Section: Discussionmentioning

confidence: 99%

Use of Acyclovir for Suppression of Human Immunodeficiency Virus Infection Is Not Associated with Genotypic Evidence of Herpes Simplex Virus Type 2 Resistance to Acyclovir: Analysis of Specimens from Three Phase III Trials

et al. 2010

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Herpes simplex virus type 2 (HSV-2) is the most common cause of genital ulcer disease and is a cofactor forHIV-1 acquisition and transmission. We analyzed specimens from three separate phase III trials of acyclovir (ACV) for prevention of HIV-1 acquisition and transmission to determine if failure of ACV to interrupt HIV acquisition and transmission was associated with genotypic ACV resistance. Acyclovir (400 mg twice daily) or placebo was provided to HSV-2-infected persons at risk of HIV-1 infection in the Mwanza and HPTN 039 trials and to persons dually infected with HSV-2 and HIV-1 who had an HIV-negative partner in the Partners in Prevention study. We extracted HSV DNA from genital ulcer swabs or cervicovaginal lavage fluids from 68 samples obtained from 64 participants randomized to ACV and sequenced the HSV-2 UL23 gene encoding thymidine kinase. The UL23 sequences were compared with published and unpublished data. Variants were observed in 38/1,128 (3.4%) nucleotide positions in the UL23 open reading frame, with 58% of these encoding amino acid changes. No deletions, insertions, or mutations known to be associated with resistance were detected. Thirty-one of the variants (81.5%) are newly reported, 15 of which code for amino acid changes. Overall, UL23 is highly polymorphic compared to other loci in HSV-2, but no drug resistance mutations were detected that could explain the failure to reduce HIV incidence or to prevent HIV-1 transmission in these studies.Herpes simplex virus type 2 (HSV-2) is one of the most common sexually transmitted infections. The prevalence of infection is higher in many parts of the developing world, especially in some settings in sub-Saharan Africa, where up to 75 to 80% of women may be infected by the age of 35 years (26).The standard treatment for symptomatic primary and recurrent genital herpes and for suppression of genital herpes has primarily been acyclovir (ACV), a guanosine nucleoside analogue that inhibits replication of HSV. The inactive prodrug is phosphorylated to ACV triphosphate by HSV-encoded thymidine kinase. The active ACV triphosphate then inhibits viral DNA polymerase. Thymidine kinase is encoded by the HSV UL23 gene. The frequency of ACV resistance is increased in ACV-treated, immunosuppressed individuals and may reach 5% (25). However, ACV resistance has also occasionally been documented in immunocompetent persons in both the absence and presence of ACV therapy (8, 28a). Up to 95% of clinically significant ACV resistance is caused by mutations in the UL23 gene that limit thymidine kinase enzymatic activity and thus prevent initial phosphorylation of the drug (1a). These are typically insertions or deletions of a single nucleotide in a poly(G) or poly(C) tract, leading to a frameshifted open reading frame with a carboxy-terminal nonsense polypeptide and premature termination (1a). Point mutations that prevent or reduce recognition of ACV as a substrate occur at lower frequencies (1a). Compared to the much greater understanding of human cytomegalovirus (CMV) and g...

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“…Furthermore, LAMP is more stable than PCR and qPCR (Francois et al, 2011). As the presence of exogenous DNA and inhibitors in clinical samples has less impact on the sensitivity of LAMP than PCR, DNA purification from samples for LAMP detection may be omitted (de Franchis et al, 1988, Kaneko et al, 2007. A cold chain is essential when preparing the master mix for PCR, while it is not mandatary in the case of LAMP.…”

Section: Discussionmentioning

confidence: 99%

“…Loop-mediated isothermal amplification (LAMP) assays rely on auto-cycling strand displacement DNA synthesis in the presence of Bst DNA polymerase under isothermal conditions within 60 min (Notomi et al, 2000;Ushikubo, 2004). In contrast to Taq DNA polymerase used in PCR, the Bst DNA polymerase is resistant to inhibitors present in crude biological samples (Kaneko et al, 2007). As four or six specific primers that recognize six or eight distinct sequences on the target DNA are required, LAMP has been shown to amplify target DNA with high specificity and is widely used in the clinical diagnosis of epidemic bacteria Knight et al, 2014), viruses (Poon et al, 2004;Curtis et al, 2014), parasites (Li et al, 2012;Ni et al, 2014) and fetal sex identification (Fu et al, 2011), as well as detection of the hypervirulent strain and toxin types of C. difficile (Kato et al, 2005;Norén et al, 2011;Boyanton et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Rapid detection of ermB gene in Clostridium difficile by loop-mediated isothermal amplification

Lin

Liu

Wang

et al. 2015

Journal of Medical Microbiology

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Macrolide-lincosamide-streptogramin B resistance in Clostridium difficile is mostly due to the ermB resistance determinant. Here, we describe a sensitive and rapid molecular method to detect ermB in C. difficile to contribute to the wider epidemiological study. Five sets of loop-mediated isothermal amplification (LAMP) primers were designed and optimized for rapid detection of ermB. The specificity and sensitivity of the primers for ermB were detected, and the ermB LAMP assay was compared to conventional PCR with 80 clinical isolates of C. difficile. Real-time monitoring of turbidity and chromogenic reaction were used to determine negative and positive results. A total of 26 pathogenic bacterial strains of different species were found to be negative for ermB, which indicated the high specificity of the primers. ermB was detected in 78.8 % (63/80) of the clinical isolates by both LAMP and conventional PCR. The detection limit of LAMP was 36.1 pg DNA ml 21 and its sensitivity was 10-fold greater than that of conventional PCR. This study is the first report regarding the development and application of the LAMP assay for detection of the ermB gene in C. difficile strains. The developed LAMP method is sensitive, specific and provides a user-friendly visual approach for the rapid detection of ermB-bearing C. difficile. Received 27 March 2015Accepted 13 June 2015 INTRODUCTIONClostridium difficile is a causative agent of antibiotic-associated diarrhoea and pseudomembranous colitis, usually as a consequence of antimicrobial therapy. During the last few decades, C. difficile infection (CDI) has become more severe, more recurrent, more resistant to antibiotics and more refractory to standard treatment, which poses a significant burden on patients, healthcare systems and society in general. Estimates suggest that the annual costs for management of CDI amount to more than $3 billion in the USA and J3 billion in Europe (Bouza, 2012;McGlone et al., 2012). Major risk factors for CDI include hospitalization, advanced age and antibiotic exposure, the latter including clindamycin and erythromycin (Aziz et al., 2001;Gerding, 1989;Kelly et al., 1994;Slimings & Riley, 2014). The majority of epidemic isolates are resistant to clindamycin, erythromycin, broad-spectrum cephalosporins and fluoroquinolones (Johnson et al., 1999; Spigaglia et al., 2011;Slimings & Riley, 2014). Thus, resistance to clindamycin and erythromycin, two antibiotics of the macrolidelincosamide-streptogramin B (MLSB) group, would further increase the risk of CDI.In C. difficile, resistance to the MLSB group of antibiotics is mainly encoded by the ermB resistance determinant. The ermB gene encodes a 23S rRNA methyltransferase that modifies the target site for the antibiotic and is located on a specific mobilizable non-conjugative element, Tn5398 (Farrow et al., 2001). However, the ermB gene is located on elements other than Tn5398 in the majority of clinical isolates. In total, 17 genetic organizations of such elements 3These authors contributed equally to this work...

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Discrimination of Herpes Simplex Virus Type 2 Strains by Nucleotide Sequence Variations

Cited by 9 publications

References 13 publications

Impact of HIV‐1 infection on herpes simplex virus type 2 genetic variability among co‐infected individuals

Impact of HIV‐1 infection on herpes simplex virus type 2 genetic variability among co‐infected individuals

Use of Acyclovir for Suppression of Human Immunodeficiency Virus Infection Is Not Associated with Genotypic Evidence of Herpes Simplex Virus Type 2 Resistance to Acyclovir: Analysis of Specimens from Three Phase III Trials

Rapid detection of ermB gene in Clostridium difficile by loop-mediated isothermal amplification

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