Varicella-Zoster Virus DNA from Persistently Infected Cells Contains Novel Tandem Duplications

Dohner, Dennis E.; Adams, Susan G.; Gelb, Lawrence D.

doi:10.1099/0022-1317-69-9-2229

Cited by 9 publications

(3 citation statements)

References 23 publications

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“…In addition intra-clade diversity has been calculated to be 0.03-0.07% or 1 in 1429-1 in 3333 bases, using sequences from 8 clade 1 viruses [13]. Whole genome sequencing also confirms early experiments showing recombination between different strains [3,14]…”

Section: Introductionmentioning

confidence: 62%

Molecular Genetic Insights Into Varicella Zoster Virus (VZV), the vOka Vaccine Strain, and the Pathogenesis of Latency and Reactivation

Breuer

2018

The Journal of Infectious Diseases

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Genetic tools for molecular typing of varicella zoster virus (VZV) have been used to understand the spread of virus, to differentiate wild-type and vaccine strains, and to understand the natural history of VZV infection in its cognate host. Molecular genetics has identified 7 clades of VZV (1-6 and 9), with 2 more mooted. Differences between the vOka vaccine strain and wild-type VZVs have been used to distinguish the cause of postimmunization events and to provide insight into the natural history of VZV infections. Importantly molecular genetics has shown that reinfection with establishment of latency by the reinfecting strain is common, that dual infections with different viruses can occur, and that reactivation of the superinfecting genotype can both occur. Whole-genome sequencing of the vOka vaccine has been used to show that vesicles form from a single virion, that latency is established within a few days of inoculation, and that all vaccine strains are capable of establishing latency and reactivating. Novel molecular tools have characterized the transcripts expressed during latent infection in vitro.

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Section: Introductionmentioning

confidence: 62%

Molecular Genetic Insights Into Varicella Zoster Virus (VZV), the vOka Vaccine Strain, and the Pathogenesis of Latency and Reactivation

Breuer

2018

The Journal of Infectious Diseases

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“…The ability of herpesviruses to establish persistent infection has been well documented (10,13,14,31,39,48). Numerous studies from our laboratory have demonstrated that DIPs of EHV-1 mediate persistent infection (2,3,8,11,26,35,41).…”

Section: Discussionmentioning

confidence: 99%

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Harty

Holden

O’Callaghan

1993

J Virol

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Defective interfering particles (DIPs) of equine herpesvirus 1 (EHV-1; Kentucky A strain) mediate persistent infection. DNA sequences at the L terminus, which contain the UL2 gene (homolog of ULS5 of herpes simplex virus type 1 and open reading frame 3 of varicella-zoster virus) of standard EHV-1, have been shown to be highly conserved in all clones of the EHV-1 DIP genome. The UL2 mRNA was characterized by Si nuclease analyses, which mapped the 5' and 3' termini of the 0.9-kb early UL2 mRNA to approximately 26 and 16 nucleotides downstream of a TITAAA box and polyadenylation signal, respectively. The UL2 open reading frame, present within both the EHV-1 standard and DIP genomes, was inserted into the transcription expression vector pGEM-3Z to yield constructs pGEML2 and pDIL2, respectively. After in vitro transcription and translation, both constructs yielded a comigrating 23-kDa protein, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Polyclonal antiserum was raised against the UL2 protein by injecting rabbits with a TrpE/UL2 fusion protein expressed from plasmid pATH23L2 in Escherichia coli. The UL2-specific antiserum reacted in Western immunoblot and immunoprecipitation analyses with a 23-kDa polypeptide synthesized in cells infected with standard EHV-1 or DIP-enriched virus. These data also indicated that the UL2 polypeptide was more abundant in DIP-infected cells than in standard EHV-1-infected cells. Results from time course and pulse-chase analyses suggested that the UL2 polypeptide has a rapid turnover rate in DIP-infected cells.

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“…While some investigators have documented changes in VZV restriction profiles on serial passage (11,12,20,45,47), others failed to observe any differences after as many as 33 passages in cultured cells (20,45). The serial passage of the Oka parental virus in tissue culture resulted in a well-documented accumulation of mostly single point mutations (20).…”

mentioning

confidence: 99%

Global Identification of Three Major Genotypes of Varicella-Zoster Virus: Longitudinal Clustering and Strategies for Genotyping

Loparev

González

DeLeon-Carnes

et al. 2004

J Virol

140

252

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By analysis of a single, variable, and short DNA sequence of 447 bp located within open reading frame 22 (ORF22), we discriminated three major varicella-zoster virus (VZV) genotypes. VZV isolates from all six inhabited continents that showed nearly complete homology to ORF22 of the European reference strain Dumas were assigned to the European (E) genotype. All Japanese isolates, defined as the Japanese (J) genotype, were identical in the respective genomic region and proved the most divergent from the E strains, carrying four distinct variations. The remaining isolates carried a combination of E-and J-specific variations in the target sequence and thus were collectively termed the mosaic (M) genotype. Three hundred twenty-six isolates collected in 27 countries were genotyped. A distinctive longitudinal distribution of VZV genotypes supports this approach. Among 111 isolates collected from European patients, 96.4% were genotype E. Consistent with this observation, approximately 80% of the VZV strains from the United States were also genotype E. Similarly, genotype E viruses were dominant in the Asian part of Russia and in eastern Australia. M genotype viruses were strongly dominant in tropical regions of Africa, Indochina, and Central America, and they were common in western Australia. However, genotype M viruses were also identified as a minority in several countries worldwide. Two major intertypic variations of genotype M strains were identified, suggesting that the M genotype can be further differentiated into subgenotypes. These data highlight the direction for future VZV genotyping efforts. This approach provides the first simple genotyping method for VZV strains in clinical samples.Varicella-zoster virus (VZV) is a human herpesvirus that commonly causes chicken pox (varicella), usually in young children. Following primary infection a lifelong latent infection is established, and the virus often reactivates in adulthood or senescence to cause shingles (zoster). The VZV genome consists of 125 kb of linear, double-stranded DNA comprising one long and one short unique region, each flanked by inverted repeats (10), and five internal repeat regions (R1 to R5) have been identified. The VZV genome contains at least 71 open reading frames (ORFs), and the functions of many of the proteins they encode have been characterized (10).During the past 2 decades, several groups attempted to evaluate VZV phylogeny. Early efforts in VZV typing used DNA restriction fragment length polymorphism (RFLP) analysis (13,37,38), an approach that confirmed the identity of the VZV strain that causes varicella on primary infection and later reactivates to cause zoster. Relatively consistent restriction enzyme digestion profiles for different VZV strains were observed, providing the first evidence that VZV has a highly conserved genome. Intrastrain variation in restriction enzyme fragment profiles among wild-type VZV isolates was observed (22,36,37). However, the most prominent differences were linked to variation in the number and composi...

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Varicella-Zoster Virus DNA from Persistently Infected Cells Contains Novel Tandem Duplications

Cited by 9 publications

References 23 publications

Molecular Genetic Insights Into Varicella Zoster Virus (VZV), the vOka Vaccine Strain, and the Pathogenesis of Latency and Reactivation

Molecular Genetic Insights Into Varicella Zoster Virus (VZV), the vOka Vaccine Strain, and the Pathogenesis of Latency and Reactivation

Transcriptional and translational analyses of the UL2 gene of equine herpesvirus 1: a homolog of UL55 of herpes simplex virus type 1 that is maintained in the genome of defective interfering particles

Global Identification of Three Major Genotypes of Varicella-Zoster Virus: Longitudinal Clustering and Strategies for Genotyping

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