Modelling the impact of a combined varicella and zoster vaccination programme on the epidemiology of varicella zoster virus in England

Vaccine ◽  
2011 ◽  
Vol 29 (13) ◽  
pp. 2411-2420 ◽  
Author(s):  
Albert Jan van Hoek ◽  
Alessia Melegaro ◽  
Emelio Zagheni ◽  
W. John Edmunds ◽  
Nigel Gay
Keyword(s):  
Varicella Zoster Virus ◽  
Vaccination Programme ◽  
Varicella Zoster ◽  
The Impact

Modelling the impact of vaccination on the epidemiology of varicella zoster virus in Australia

2005 ◽  
Vol 29 (6) ◽  
pp. 544-551 ◽  
Author(s):  
Heather F. Gidding ◽  
Marc Brisson ◽  
C. Raina Macintyre ◽  
Margaret A. Burgess
Keyword(s):  
Varicella Zoster Virus ◽  
Varicella Zoster ◽  
The Impact

Modelling the impact of one-dose vs. two-dose vaccination regimens on the epidemiology of varicella zoster virus in Australia

2009 ◽  
Vol 138 (4) ◽  
pp. 457-468 ◽  
Author(s):  
Z. GAO ◽  
H. F. GIDDING ◽  
J. G. WOOD ◽  
C. R. MacINTYRE
Keyword(s):  
Mathematical Model ◽  
Varicella Zoster Virus ◽  
Vaccination Strategy ◽  
Vaccination Schedule ◽  
Varicella Zoster ◽  
Dose Strategy ◽  
Vaccination Strategies ◽  
Age Of Infection ◽  
The Impact

SUMMARYWe examined the impact of one-dose vs. two-dose vaccination strategies on the epidemiology of varicella zoster virus (VZV) in Australia, using a mathematical model. Strategies were assessed in terms of varicella (natural and breakthrough) and zoster incidence, morbidity, average age of infection and vaccine effectiveness (VE). Our modelling results suggest that compared to a one-dose vaccination strategy (Australia's current vaccination schedule), a two-dose strategy is expected to not only produce less natural varicella cases (5% vs. 13% of pre-vaccination state, respectively) but also considerably fewer breakthrough varicella cases (only 11·4% of one-dose strategy). Therefore a two-dose infant vaccination programme would be a better long-term strategy for Australia.

scholarly journals Varicella-Zoster Virus ORF63 Inhibits Apoptosis of Primary Human Neurons

2006 ◽  
Vol 80 (2) ◽  
pp. 1025-1031 ◽  
Author(s):  
Chantelle Hood ◽  
Anthony L. Cunningham ◽  
Barry Slobedman ◽  
Ann M. Arvin ◽  
Marvin H. Sommer ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Sensory Neurons ◽  
Human Fibroblasts ◽  
Late Phase ◽  
Annexin V ◽  
Viral Gene ◽  
Gene Encoding ◽  
Varicella Zoster ◽  
Human Neurons ◽  
The Impact

ABSTRACT Virus-encoded modulation of apoptosis may serve as a mechanism to enhance cell survival and virus persistence. The impact of productive varicella-zoster virus (VZV) infection on apoptosis appears to be cell type specific, as infected human sensory neurons are resistant to apoptosis, yet human fibroblasts readily become apoptotic. We sought to identify the viral gene product(s) responsible for this antiapoptotic phenotype in primary human sensory neurons. Treatment with phosphonoacetic acid to inhibit viral DNA replication and late-phase gene expression did not alter the antiapoptotic phenotype, implicating immediate-early (IE) or early genes or a virion component. Compared to the parental VZV strain (rOKA), a recombinant virus unable to express one copy of the diploid IE gene ORF63 (rOkaΔORF63) demonstrated a significant induction of apoptosis in infected neurons, as determined by three methods: annexin V staining, deoxynucleotidyltransferase-mediated dUTP-biotin nick end label staining, and transmission electron microscopy. Furthermore, neurons transfected with a plasmid expressing ORF63 resisted apoptosis induced by nerve growth factor withdrawal. These results show that ORF63 can suppress apoptosis of neurons and provide the first identification of a VZV gene encoding an antiapoptotic function. As ORF63 is expressed in neurons during both productive and latent infection, it may play a significant role in viral pathogenesis by promoting neuron survival during primary and reactivated infections.

Varicella in Children With Cancer: Impact of Antiviral Therapy and Prophylaxis

PEDIATRICS ◽  
1987 ◽  
Vol 80 (4) ◽  
pp. 465-472
Author(s):  
Sandor Feldman ◽  
Lennie Loft
Keyword(s):  
Mortality Rate ◽  
Acute Leukemia ◽  
Varicella Zoster Virus ◽  
Antiviral Therapy ◽  
Passive Immunization ◽  
Skin Lesions ◽  
Children With Cancer ◽  
Varicella Zoster ◽  
Adenine Arabinoside ◽  
The Impact

To estimate the impact of antiviral therapy and prophylaxis on the natural course of the infection, 288 cases of varicella in children with cancer were reviewed. Among 127 patients with untreated infections, the overall mortality rate was 7%. Varicella-zoster virus pneumonitis developed in 28% of the untreated patients and was associated with a 25% mortality rate. Pneumonitis was much more likely to develop in patients with acute leukemia than in those with other malignancies (32% v 19%). Similarly, deaths due to pneumonitis were restricted to patients with acute leukemia. Lymphopenia (absolute lymphocyte count <500/µL) was significantly associated with varicella-zoster virus pneumonitis and a higher fatality rate among patients with this complication. Both acyclovir and adenine arabinoside, administered to 18 and 28 patients, respectively, stopped the progression of skin lesions; however, pneumonitis developed in none of the acyclovir recipients after two days of treatment, compared with 29% of the adenine arabinoside recipients (P = .03). Passive immunization in 45 children who subsequently had varicella was associated with an 11% incidence of varicella-zoster virus pneumonitis. Despite passive immunization of approximately 150 children, the attack rate of varicella at our institution remains unchanged. Results of this study demonstrate the efficacy of antiviral therapy and passive immunization in patients with childhood cancer and varicella, but prevention of the infection will require a universal vaccine.

scholarly journals Inhibition of integrin α6 expression by cell-free varicella-zoster virus

2012 ◽  
Vol 93 (8) ◽  
pp. 1725-1730 ◽  
Author(s):  
Joshua B. Bowles ◽  
Megan Steain ◽  
Barry Slobedman ◽  
Allison Abendroth
Keyword(s):  
Varicella Zoster Virus ◽  
Nuclear Dna ◽  
Natural Infection ◽  
Surface Protein ◽  
Varicella Zoster ◽  
Human Foreskin Fibroblasts ◽  
Surface Protein Expression ◽  
Post Entry ◽  
Simplex Virus ◽  
The Impact

Varicella-zoster virus (VZV) causes chickenpox and shingles. VZV is released from infected cells during natural infection, but remains highly cell-associated during experimental infection, and so most studies have utilized cell-associated infection models. We examined the impact of cell-free VZV infection of primary human foreskin fibroblasts (HFFs) on the receptor integrin α6 (ITGA6). qPCR and flow cytometry demonstrated that both cell-free VZV and cell-free UV-inactivated VZV downregulated transcription and cell-surface protein expression of ITGA6. To establish whether ITGA6 altered VZV infection, VZV transcripts and nuclear DNA levels were measured in HFFs treated with ITGA6 blocking antibody before infection. ITGA6 blocking did not impair virus entry but did negatively impact VZV transcription, and this effect was virus specific as transcription of the related herpes simplex virus type 1 was not similarly inhibited. This study identifies modulation of ITGA6 during cell-free VZV infection, and provides the first evidence linking ITGA6 with post-entry productive VZV gene expression.

Varicella-Zoster Virus

2018 ◽  
Author(s):  
Olivier Picone ◽  
Christelle Vauloup-Fellous ◽  
Laurent Mandelbrot
Keyword(s):  
Varicella Zoster Virus ◽  
Early Recognition ◽  
Varicella Vaccine ◽  
Skin Lesions ◽  
Varicella Infection ◽  
Varicella Zoster ◽  
Mother And Child ◽  
Life Threatening ◽  
Peripartum Period ◽  
The Impact

Chickenpox in a pregnant woman is uncommon, but it is a major concern for patients and their families, as well as for clinicians caring for pregnant women. Varicella infection during pregnancy is usually benign, but there can be serious consequences for both mother and child. Notably, fetal varicella syndrome (FVS) can happen when infection occurs before 21 weeks of gestation. It can present with serious neurological anomalies and unusual cicatricial skin lesions. Later in pregnancy, primary neonatal varicella may occur when the mother is infected in the peripartum period, and it can be life-threatening. The complications of varicella during pregnancy are reviewed, with an emphasis on early recognition, accurate timing of infection, and risk to the developing fetus and newborn infant. The impact of varicella vaccine on the epidemiology of these infections is reviewed, as well as indications for varicella-zoster virus (VZV)–specific immune globulin and antiviral therapy with acyclovir.

scholarly journals Infection and Functional Modulation of Human Monocytes and Macrophages by Varicella-Zoster Virus

2018 ◽  
Vol 93 (3) ◽  
Author(s):  
Jarrod J. Kennedy ◽  
Megan Steain ◽  
Barry Slobedman ◽  
Allison Abendroth
Keyword(s):  
Cell Surface ◽  
Varicella Zoster Virus ◽  
Immune Cells ◽  
Human Fibroblasts ◽  
Immunofluorescent Staining ◽  
Human Monocytes ◽  
Varicella Zoster ◽  
Monocytes And Macrophages ◽  
The Impact ◽  
Human Monocytes And Macrophages

ABSTRACTVaricella-zoster virus (VZV) is associated with viremia during primary infection that is presumed to stem from infection of circulating immune cells. While VZV has been shown to be capable of infecting a number of different subsets of circulating immune cells, such as T cells, dendritic cells, and NK cells, less is known about the interaction between VZV and monocytes. Here, we demonstrate that blood-derived human monocytes are permissive to VZV replicationin vitro. VZV-infected monocytes exhibited each temporal class of VZV gene expression, as evidenced by immunofluorescent staining. VZV virions were observed on the cell surface and viral nucleocapsids were observed in the nucleus of VZV-infected monocytes by scanning electron microscopy. In addition, VZV-infected monocytes were able to transfer infectious virus to human fibroblasts. Infected monocytes displayed impaired dextran-mediated endocytosis, and cell surface immunophenotyping revealed the downregulation of CD14, HLA-DR, CD11b, and the macrophage colony-stimulating factor (M-CSF) receptor. Analysis of the impact of VZV infection on M-CSF-stimulated monocyte-to-macrophage differentiation demonstrated the loss of cell viability, indicating that VZV-infected monocytes were unable to differentiate into viable macrophages. In contrast, macrophages differentiated from monocytes prior to exposure to VZV were highly permissive to infection. This study defines the permissiveness of these myeloid cell types to productive VZV infection and identifies the functional impairment of VZV-infected monocytes.IMPORTANCEPrimary VZV infection results in the widespread dissemination of the virus throughout the host. Viral transportation is known to be directly influenced by susceptible immune cells in the circulation. Moreover, infection of immune cells by VZV results in attenuation of the antiviral mechanisms used to control infection and limit spread. Here, we provide evidence that human monocytes, which are highly abundant in the circulation, are permissive to productive VZV infection. Furthermore, monocyte-derived macrophages were also highly permissive to VZV infection, although VZV-infected monocytes were unable to differentiate into macrophages. Exploring the relationships between VZV and permissive immune cells, such as human monocytes and macrophages, elucidates novel immune evasion strategies and provides further insight into the control that VZV has over the immune system.

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