Molecular studies of Varicella zoster virus

Quinlivan, Mark; Breuer, Judith

doi:10.1002/rmv.502

Cited by 56 publications

(47 citation statements)

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“…Although our isolates had no such mutations, exogenic reinfection may occur in immunocompetent and immunocompromised individuals, and recombinant virus could be released during subclinical virus replication or a shingles episode. Both serologic evidence and confirmed cases of reinfection with VZV have been described (3,13,40; see also the review of Quinlivan and Breuer [39]). Another open question is the mechanism of recombination.…”

Section: Genotyping Of Vzv Field Isolatesmentioning

confidence: 88%

Sequencing of 21 Varicella-Zoster Virus Genomes Reveals Two Novel Genotypes and Evidence of Recombination

Zell

Taudien

Pfaff

et al. 2012

J Virol

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Genotyping of 21 varicella-zoster virus (VZV) strains using a scattered single nucleotide polymorphism (SNP) method revealed ambiguous SNPs and two nontypeable isolates. For a further genetic characterization, the genomes of all strains were sequenced using the 454 technology. Almost-complete genome sequences were assembled, and most remaining gaps were closed with V aricella-zoster virus (VZV) is a member of the genus Varicellovirus within the subfamily Alphaherpesvirinae, family Herpesviridae (8). The alphaherpesviruses are characterized by their short reproduction cycle, fast spreading, efficient destruction of infected cells, and persistence in sensory ganglia. VZV replication is limited exclusively to cells of human and simian origins. The VZV genome consists of double-stranded DNA with a size of 125 kb and comprises 73 genes, 70 of which are unique and 3 of which are duplicated (9). The virus genome includes two main coding regions, unique long (U L ) and unique short (U S ), and flanking inverted repeats, termed terminal and internal repeats long (TR L , IR L ) and short (TR S , IR S ). In addition to these repeats, there are five genomic regions with tandem reiterations, designated R1 to R5.Primary infection with VZV causes varicella (chickenpox), a condition characterized by fever and exanthema with small blisters. Virus uptake occurs via the mucous membranes of the respiratory tract, with primary replication seen in the regional lymph nodes. During a short phase of primary cell-associated viremia, the virus infects peripheral blood mononuclear cells. In a secondary viremia, the virus spreads to cutaneous epithelial cells, where it induces rash. Usually, the virus is spread by excretion of aerosolized virus particles from the respiratory tract and highly infectious vesicle fluid from rash (2). After primary infection, VZV establishes a lifelong latency in trigeminal and dorsal root ganglia. Endogenous viral reactivation, e.g., after decline of VZV-specific cell-mediated immunity, may lead to viral replication and inflammation in the ganglion. Then, progeny virus migrates along the axons of neurons and is released in the skin, where it causes herpes zoster (shingles). Zoster is characterized by a unilateral vesicular rash within a single cutaneous dermatome. In most cases, the thoracic region is involved.Genetic characterization of VZV DNA is achieved by analysis of restriction fragment length polymorphism (RFLP), single nucleotide polymorphisms (SNPs), and full-genome sequencing. Early RFLP analyses revealed both interstrain variations among wild-type isolates and differences between wild-and vaccine-type viruses. The most commonly used RFLP markers of VZV included the polymorphism of open reading frames (ORFs) 38 (PstI), 54 (BglI), and 62 (SmaI) (19,23,45). These markers allowed the majority of wild-type strains in North America and Europe to be typed as PstI ϩ BglI Ϫ , whereas African and Asian strains were BglI ϩ and Japanese Oka-like wild-type strains were PstI ϩ /PstI Ϫ BglI ϩ SmaI Ϫ ; the Oka vacc...

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Section: Genotyping Of Vzv Field Isolatesmentioning

confidence: 88%

Sequencing of 21 Varicella-Zoster Virus Genomes Reveals Two Novel Genotypes and Evidence of Recombination

Zell

Taudien

Pfaff

et al. 2012

J Virol

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“…At least for four of the six patients, the rise of anti-VZV IgG levels was not accompanied by herpes zoster nor other clinical symptoms of VZV disease, indicating subclinical reactivation or reinfection in these cases. Evidence of subclinical reactivation of VZV was previously obtained by measuring significant rises of anti-VZV IgG levels after household exposure of seropositive individuals (reviewed in Quinlivan and Breuer) 24 ; by detection of VZV DNA, in patients with malignancies without clinical symptoms of VZV disease 38 ; and by intrathecal synthesis of anti-VZV antibodies in the absence of a history of herpes zoster, in HIV-infected individuals. 39 In a long-term longitudinal study, with a follow-up of 45 healthy subjects for up to 26 years, it was observed that there were rises of anti-VZV antibody levels by more than 2-fold, with an incidence of 1.6 events per 100 person-years.…”

Section: Discussionmentioning

confidence: 99%

Serological evidence of increased susceptibility to varicella-zoster virus reactivation or reinfection in natalizumab-treated patients with multiple sclerosis

et al. 2015

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Background: Serious adverse drug reactions of disease-modifying drugs in multiple sclerosis (MS) therapy may include enhanced susceptibility to reactivation of neurotropic herpes viruses like varicella-zoster virus (VZV) and the John Cunningham (JC) polyomavirus. Objective: Because symptomatic reactivation of these viruses are rare events, we determined the incidence of rises in anti-VZV IgG antibody levels as a potential marker for enhanced susceptibility to subclinical and symptomatic reactivation of neurotropic viruses. Methods: Anti-VZV IgG levels were measured in paired serum samples taken 6-8 months apart from natalizumab-treated MS patients, healthy blood donors and human immunodeficiency virus (HIV) infected patients. Results: The incidence of significant rises in anti-VZV IgG levels in natalizumab-treated MS patients was 4.26 per 100 person-years, which was significantly higher than in healthy blood donors. Retrospective evaluation of the available medical records of patients with rises of anti-VZV IgG levels did not reveal herpes zoster (i.e. shingles) manifestations. Conclusions:The increased incidence of significant rises of anti-VZV IgG levels in natalizumab-treated MS patients might indicate an association of natalizumab treatment of MS with an elevated risk of a subclinical VZV reactivation and/or reinfection events. Whether this is predictive of an increased risk of herpes zoster or even symptomatic reactivation of other neurotropic viruses remains to be determined in larger prospective studies.

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“…However, to date it is not clear that these mutations play an important role in the attenuation of vOka (1,5). In this study, ORF 62 of VZV wild-type strains was analyzed by DNA sequencing.…”

Section: Varicella-zoster Virus Strains Of European Genotypes Have Dementioning

confidence: 99%

Variability of Immediate-Early Gene 62 in German Varicella-Zoster Virus Wild-Type Strains

et al. 2009

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Varicella-zoster virus strains of European genotypes have developed a high variability of open reading frame(ORF) 62 during their occurrence over many years in Germany. M1 strains in Germany display a uniform ORF 62 pattern, suggesting that these strains were introduced from Africa and/or Asia via few sources during the last years.During the surveillance of circulating varicella-zoster virus (VZV) strains, the analysis of the immediate-early gene 62 region has an important function, since 15 of the described 42 vaccine mutations of the Oka vaccine strain (vOka) were found in open reading frame (ORF) 62 alone. However, to date it is not clear that these mutations play an important role in the attenuation of vOka (1,5). In this study, ORF 62 of VZV wild-type strains was analyzed by DNA sequencing. The primary objective was to search for both genotypic markers and vaccine-related mutations.The study included 86 VZV isolates from 59 patients with varicella and 27 patients with zoster. Patients were randomly selected between 2003 and 2007, as described previously (8, 10). No patient had received a varicella vaccination. All patients or their parents gave the consent for the specimen collection. VZV isolates were cultured for two to four passages (9), genotyped (10), and stored at Ϫ80°C. For sequencing of ORF 62, DNA was isolated by means of a QIAamp blood kit (Qiagen, Hilden, Germany) and amplified using High-Fidelity enzyme mix (Fermentas, St.-Leon-Rot, Germany). The amplification mixture contained 10 M of each primer (Table 1; ORF 62, VZV-4F and VZV-26R; fragment A, VZV-25F and VZV-10R; fragment B, VZV-9F and VZV-17R) plus approximately 50 ng template DNA per 50 l. Reaction mixtures were cycled 35 times at 95°C for 40 s, at 55°C (ORF 62, fragment A) or 50°C (fragment B) for 45 s, and at 68°C for 1 min/kbp. An amount of 200 ng gel-purified DNA per l was used for the sequencing reaction, carried out by means of the cycle sequencing method using a DYEnamic ET Terminator cycle sequencing kit (Amersham Biosciences Europe, Freiburg, Germany) and 10 M oligonucleotide primers (Table 1). The thermal conditions of amplification followed 25 cycles of 95°C for 20 s, 50°C for 15 s, and 60°C for 1 s. DNA fragments were analyzed as described previously (10). Results were compared with published sequences of the reference strains Dumas (genotype E1; GenBank accession no. NC_001348 and X04370), VZV 11 (genotype E2; accession no. DQ479955), VZV CA 123 (genotype M1; accession no. DQ457052), VZV 8 (genotype M2; accession no. DQ479960), pOka (genotype J; accession no. AB097933), and vOka (genotype J; accession no. AB097932).The genotype E1 strains (Table 2), 17 from patients with varicella and 14 from patients with zoster, contained three genotype-specific nucleotides in positions 107165 (C), 108747 (A), and 108951 (G). Whereas the single nucleotide polymorphism (SNP) at nucleotide 108951 was observed in all E1 strains, the SNPs in positions 107165 and 108747 were present in 16 varicella strains (94.1%) and all zoster strains. The ...

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Molecular studies of Varicella zoster virus

Cited by 56 publications

References 223 publications

Sequencing of 21 Varicella-Zoster Virus Genomes Reveals Two Novel Genotypes and Evidence of Recombination

Sequencing of 21 Varicella-Zoster Virus Genomes Reveals Two Novel Genotypes and Evidence of Recombination

Serological evidence of increased susceptibility to varicella-zoster virus reactivation or reinfection in natalizumab-treated patients with multiple sclerosis

Variability of Immediate-Early Gene 62 in German Varicella-Zoster Virus Wild-Type Strains

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