Differentiation of Oka varicella vaccine strain from wild varicella‐zoster virus strains isolated from vaccinees and household contact

Shiraki, Kimíyasu; Horiuchi, Kensuke; Asano, Yoshizo; Yamanishi, Koichi; Takahashi, Michiaki

doi:10.1002/jmv.1890330212

Cited by 24 publications

(20 citation statements)

References 17 publications

(20 reference statements)

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“…In comparison, 19 to 20% of wild-type viruses being positive for BglI site have been found in the United Kingdom and the United States [LaRussa et al, 1992;. The identification of this BglI polymorphism in clinical isolates before the introduction of varicella vaccine indicates that this genetic alteration arose in the United States as the result of a single-base-pair mutation [LaRussa et al, 1992] and has not been created by recombination between vaccine and wild-type virus, which has been observed in vitro [Dohner et al, 1988] and in vivo [Shiraki et al, 1991]. Because of the rare detection of Oka, such recombination is also unlikely in Germany.…”

Section: Discussionmentioning

confidence: 94%

Molecular characterisation of varicella‐zoster virus strains in Germany and differentiation from the Oka vaccine strain

Sauerbrei

Eichhorn

Gawellek

et al. 2003

Journal of Medical Virology

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With the introduction of varicella vaccination, surveillance of varicella-zoster virus (VZV) strains occurring in cases of chickenpox or zoster should be considered. Differentiating Oka vaccine strain from wild-type VZV can be achieved only using molecular genotyping. In the present study, the VZV genotype was examined in 53 VZV strains isolated from patients with varicella or zoster and in 73 samples from skin eruptions, cerebrospinal fluid, and throat swabs obtained from patients with VZV infections in Germany. The polymerase chain reaction and restriction fragment length polymorphisms analysis using DNA fragments of the open reading frames 38, 54, 62, and the R5 repeat region were used. Whereas all VZV isolates could be typed, direct genotyping of viral DNA in patients' samples was achieved in 63 of 73 cases (86.3%). The dominant genotype of VZV found in 88.8% of 116 patients had the wild-type pattern PstI(+) BglI(-) R5A followed by the wild-genotype PstI(+) BglI(+) R5A in 6.0%, the wild-genotype PstI(+) BglI(-) R5B in 3.4%, the wild-genotype PstI(+) BglI(-) R5C and the Oka vaccine genotype PstI(-) BglI(+) R5B in 0.9% of patients each. BglI(-) wild-types were found in 90.7% of patients with zoster and in 9.3% of patients with varicella. By contrast, the BglI(+) wild-type was diagnosed in five patients with varicella and in two patients with zoster. In conclusion, VZV strains found in Germany are similar to strains circulating in the United States and the United Kingdom. VZV wild-type strains containing a BglI restriction site in ORF 54 as well as Oka vaccine strains can rarely be detected.

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Section: Discussionmentioning

confidence: 94%

Molecular characterisation of varicella‐zoster virus strains in Germany and differentiation from the Oka vaccine strain

Sauerbrei

Eichhorn

Gawellek

et al. 2003

Journal of Medical Virology

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“…This is partly due to a lack of efficient tools necessary for such studies; however, major technological advances in the last decade now allow those types of studies. With respect to VZV, it has been shown that recombination between the live varricella vaccine and wild-type VZV occurs during coinfection in vitro [46] and has been suggested to occur in vivo [47]. Most recently, Breuer and colleagues [39] referred to the emergence of new wild-type/vaccine recombinants by partial-genome sequencing of VZV isolates.…”

Section: Discussionmentioning

confidence: 99%

Dual Infection and Superinfection Inhibition of Epithelial Skin Cells by Two Alphaherpesviruses Co-Occur in the Natural Host

Jarosinski

2012

PLoS ONE

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Hosts can be infected with multiple herpesviruses, known as superinfection; however, superinfection of cells is rare due to the phenomenon known as superinfection inhibition. It is believed that dual infection of cells occurs in nature, based on studies examining genetic exchange between homologous alphaherpesviruses in the host, but to date, this has not been directly shown in a natural model. In this report, gallid herpesvirus 2 (GaHV-2), better known as Marek’s disease virus (MDV), was used in its natural host, the chicken, to determine whether two homologous alphaherpesviruses can infect the same cells in vivo. MDV shares close similarities with the human alphaherpesvirus, varicella zoster virus (VZV), with respect to replication in the skin and exit from the host. Recombinant MDVs were generated that express either the enhanced GFP (eGFP) or monomeric RFP (mRFP) fused to the UL47 (VP13/14) herpesvirus tegument protein. These viruses exhibited no alteration in pathogenic potential and expressed abundant UL47-eGFP or -mRFP in feather follicle epithelial cells in vivo. Using laser scanning confocal microscopy, it was evident that these two similar, but distinguishable, viruses were able to replicate within the same cells of their natural host. Evidence of superinfection inhibition was also observed. These results have important implications for two reasons. First, these results show that during natural infection, both dual infection of cells and superinfection inhibition can co-occur at the cellular level. Secondly, vaccination against MDV with homologous alphaherpesvirus like attenuated GaHV-2, or non-oncogenic GaHV-3 or meleagrid herpesvirus (MeHV-1) has driven the virus to greater virulence and these results implicate the potential for genetic exchange between homologous avian alphaherpesviruses that could drive increased virulence. Because the live attenuated varicella vaccine is currently being administered to children, who in turn could be superinfected by wild-type VZV, this could potentiate recombination events of VZV as well.

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“…Analysis of Isolated DNA Viral DNA was prepared from the nucleocapsid as described previously [Shiraki et al, 1991;Ida et al, 1999;Yoshida et al, 2005] and were subjected to RE fragment comparison. The genital, first whitlow (whitlow 1), and recurrent whitlow (whitlow 2) isolates, five strains of unrelated clinical genital HSV-2 isolates, and the 7401H HSV-1 strain Okuda et al, 2004;Yoshida et al, 2005] were compared for their epidemiological relatedness in the profiles of RE fragments of their DNA after BamHI, BglII, EcoRI, and SalI digestion.…”

Section: Restriction Endonuclease (Re)mentioning

confidence: 99%

“…The genital and two whitlow isolates were identified as HSV-2 by a Microtrack assay and the PCR products of the DNA polymerase region (data not shown). RE fragment polymorphism was used to examine the epidemiological relatedness of the genital, first, and recurrent whitlow isolates by comparison with the other clinical isolates [Buchman et al, 1978[Buchman et al, , 1980Shiraki et al, 1991]. Figure 2 shows the profiles of RE fragments of DNA from the genital and two whitlow isolates as well as HSV strains.…”

Section: Genotypic Characterization Of Genital and Two Whitlow Isolatesmentioning

confidence: 99%

Genital herpes due to acyclovir‐sensitive herpes simplex virus caused secondary and recurrent herpetic whitlows due to thymidine kinase‐deficient/temperature‐sensitive virus

Shimada

Suzuki

Shirasaki

et al. 2007

Journal of Medical Virology

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Herpes simplex virus (HSV)-2 caused a genital ulcer in a 40-year-old allogenic stem cell recipient, and a secondary herpetic whitlow appeared during 2 months of acyclovir (ACV) therapy. Both genital ulcer, and whitlow were cured 3 months later, but 6 months after recovery the whitlow alone recurred. DNA of the genital, first, and recurrent whitlow isolates showed similar endonuclease digestion fragment profiles. The genital virus was ACV-sensitive, and the two whitlow isolates were ACV-resistant/thymidine kinase (TK)-deficient. The TK gene of the whitlow isolates had the same frame shift from the 274th amino acid and termination at the 347th amino acid due to the deletion of a cytosine at the 819th nucleotide. Because the temperature of the thumb is 33/34 degrees C or lower, the temperature sensitivity of the isolates were compared, and both whitlow isolates were significantly more temperature-sensitive (ts) at 39 degrees C than the genital isolate. The two whitlow isolates showed cutaneous pathogenicity in mouse ear pinna but not midflank, while the genital isolate was pathogenic at both sites, suggesting that temperature adaptation was an important element of pathogenicity in the whitlow. The virus populations of isolates of the genital, and first whitlow were examined by 31, and 82 clones, respectively, and the clones from genital, and whitlow isolates were ACV-sensitive, and -resistant, respectively, showing their homogeneity. The acyclovir-sensitive genital lesion had spread as a TK-deficient/ts herpetic whitlow during ACV treatment, and an apparently TK-deficient virus adapted to the local temperature might have caused the whitlow recurrence.

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Differentiation of Oka varicella vaccine strain from wild varicella‐zoster virus strains isolated from vaccinees and household contact

Cited by 24 publications

References 17 publications

Molecular characterisation of varicella‐zoster virus strains in Germany and differentiation from the Oka vaccine strain

Molecular characterisation of varicella‐zoster virus strains in Germany and differentiation from the Oka vaccine strain

Dual Infection and Superinfection Inhibition of Epithelial Skin Cells by Two Alphaherpesviruses Co-Occur in the Natural Host

Genital herpes due to acyclovir‐sensitive herpes simplex virus caused secondary and recurrent herpetic whitlows due to thymidine kinase‐deficient/temperature‐sensitive virus

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