Stronger Interference of Avian Influenza Virus-Specific Than Newcastle Disease Virus-Specific Maternally Derived Antibodies with a Recombinant NDV-H5 Vaccine.

Maternally derived antibodies (MDA) are known to provide early protection from disease but also to interfere with vaccination efficacy of young chicks. This interference phenomenon is well described in the literature for viral diseases such as infectious bursal disease, Newcastle disease (ND), and avian influenza (AI). The goal of this work was to investigate the impact of H5 MDA and/or ND virus (NDV) MDA on the vaccine efficacy of a recombinant NDV-H5-vectored vaccine (rNDV-H5) against two antigenically divergent highly pathogenic AI (HPAI) H5N1 challenges.

Application of a new bivalent Marek's disease vaccine does not interfere with infectious bronchitis or Newcastle disease vaccinations and proves efficacious.

A possible interference after Marek's disease (MD) vaccination using an experimental bivalent vaccine, consisting of a redesigned CVI-988/Rispens-type MDV-1 strain and herpesvirus of turkeys, with vaccination against infectious bronchitis (IB) virus (IBV) or Newcastle disease (ND) virus (NDV) was examined. Day-old specific-pathogen-free chicks were concomitantly vaccinated with the bivalent MD vaccine (either intramuscularly or subcutaneously) and with commercially available vaccines against ND or IB. Afterward chickens were challenged with either lethal MD virus (MDV) or NDV strains or with a pathogenic IBV strain.

Potency of a recombinant NDV-H5 vaccine against various HPAI H5N1 virus challenges in SPF chickens.

For the past decade, several recombinant Newcastle disease viruses (rNDV) have been used as a vector to express native or modified avian influenza (AI) hemagglutinins (HA) in order to give preventive protection against highly pathogenic avian influenza (HPAI) H5N1 viruses. Obtained protections were dependent on the age of the chickens, on the constructs and, in particular, on the homology between the HA that was inserted and the challenge strains. The objective of this study was to investigate the vaccine efficacy of a recombinant NDV La Sota-vectored vaccine expressing an Asian clade 1 H5 ectodomain (rNDV-H5) vaccine expressing a modified H5 ectodomain from an HPAI clade 1 H5N1 isolate as vaccine for 1-day-old specific-pathogen-free chickens.

The phosphorylation profile of protein kinase A substrates is modulated during Varicella-zoster virus infection.

The cAMP-dependent protein kinase A (PKA) is a key enzyme for many cellular mechanisms. In this study, we investigated the importance of this kinase for the replication of the alphaherpesvirus Varicella-zoster virus (VZV). We report that the expression of the catalytic subunit of PKA was strongly increased at the beginning of the viral cycle.

Varicella-zoster virus infection induces the secretion of interleukin-8.

Interleukin-8 (IL-8) is an important mediator in neutrophil-mediated acute inflammation but has also a wide range of actions on various cells types. We demonstrated that infection of melanoma cells and fibroblasts with cell-associated varicella-zoster virus (VZV) and infection of a T cell line with cell-free VZV resulted in an induction of IL-8 secretion in vitro. The inhibition of the VZV replication with a drug interfering with its DNA replication had no effect on the IL-8 release.

Varicella-zoster virus requires a functional PI3K/Akt/GSK-3alpha/beta signaling cascade for efficient replication.

Successful replication of Varicella-zoster virus (VZV) relies upon strategies to counteract host defense mechanisms. This can be achieved by modulating host cell signaling pathways, which regulate apoptosis and cell survival. The Akt cascade is crucial for the regulation of cell survival since it controls factors such as Bad, FOXO1, mTor and GSK-3alpha/beta.

Varicella-zoster virus influences the activities of components and targets of the ERK signalling pathway.

Varicella-zoster virus (VZV) is ultimately dependent upon its host cell for replication. To ensure its reproduction, VZV reorganizes various cellular functions by taking advantage of pre-existing signalling pathways. Recently, it was demonstrated that the activation of stress-related mitogen-activated protein kinase pathways following infection led to increased phosphorylation of cellular transcription factors involved in VZV gene expression.

The varicella-zoster virus-mediated delayed host shutoff: open reading frame 17 has no major function, whereas immediate-early 63 protein represses heterologous gene expression.

We reported that varicella-zoster virus (VZV) causes a delayed host shutoff during its replicative cycle. VZV open reading frame 17 (ORF17) is the homologue of the herpes simplex virus (HSV) UL41 gene encoding the virion host shutoff (vhs) protein which is responsible for the shutoff effect observed in HSV-infected cells. In the present study, we demonstrated that ORF17 is expressed as a late protein during the VZV replicative cycle in different infected permissive cell lines which showed a delayed shutoff of cellular RNA.

Varicella-zoster virus infection influences expression and organization of actin and alpha-tubulin but does not affect lamin A and vimentin.

Objective: The aim of this study was to examine the effects of varicella-zoster virus (VZV) infection on the cytoskeletal components actin, lamin A, alpha-tubulin and vimentin.

Methods: The expression patterns of these four proteins during VZV infection were studied by Northern and Western blotting. The filaments were also studied in their cellular environment by immunofluorescence using confocal microscopy.

ORF61 protein of Varicella-zoster virus influences JNK/SAPK and p38/MAPK phosphorylation.

Recently, it was demonstrated that the Varicella-zoster virus (VZV) infection led to an activation of MAP kinases. The viral protein encoded by ORF61 is a major effector of JNK/SAPK and p38/MAPK phosphorylation. ORF61 shows homology to HSV-1 ICP0, a multifunctional protein that influences the activity of c-Jun in infected cells.

Role of the protein kinase PKR in the inhibition of varicella-zoster virus replication by beta interferon and gamma interferon.

Varicella-zoster virus (VZV) is sensitive to type I and type II interferons (IFNs), which mediate antiviral effects. In this study, it was demonstrated that IFN-beta and IFN-gamma inhibited the replication of VZV in vitro. Although IFN-beta was more effective than IFN-gamma, the level of inhibition of VZV replication achieved by the combination of both IFNs was more than additive and it was concluded that these two cytokines acted synergistically.

Replication of varicella-zoster virus is influenced by the levels of JNK/SAPK and p38/MAPK activation.

Stimulation of the Jun NH(2)-terminal kinase/stress-activated protein kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38/MAPK) is part of the stress-related signal transduction pathways conveying signals from the cell surface into the nucleus in order to initiate programmes of gene expression. Here, it was shown that infection by varicella-zoster virus (VZV) caused a 34-fold increase in activation of JNK/SAPK in the early phase of infection and a 2-fold increase in activation of p38/MAPK in the later phase. The phosphorylation of downstream targets c-Jun and ATF-2 was also increased; subsequent cascades to induce pro-inflammatory responses were significantly activated whereas cascades to activate apoptotic events were not.

Varicella-zoster virus does not significantly induce cell defence mechanism mediated by the 2-5A/RNase L pathway during its replication cycle.

The 2-5A/RNase L pathway belongs to the antiviral system induced by interferon (IFN). RNase L is an inactive endoribonuclease which is activated by 2'-5' oligoadenylate (2-5A) synthesized by 2',5'-oligoadenylate synthetases. Once activated, RNase L cleaves mRNA, inhibiting the protein synthesis, as well as 28S and 18S ribosomal RNA (rRNA), leading to ribosomal inactivation.

Transcription factor USF, expressed during the entire phase of varicella-zoster virus infection, interacts physically with the major viral transactivator IE62 and plays a significant role in virus replication.

The expression of the genes of varicella-zoster virus (VZV) is regulated by self-encoded viral as well as cellular transcription factors. A potential candidate with an ability to influence the transcription of VZV genes is USF (upstream stimulatory factor), which recognizes the consensus E-box motif. Quantitative RT-PCR and immunoblot assays indicate stable expression of both USF1 and USF2 throughout infection.

Implication of the product of the bovine herpesvirus type 1 UL25 gene in capsid assembly.

The UL25 ORF of bovine herpesvirus type 1 (BHV-1) was demonstrated recently to represent a gene encoding a 63 kDa viral protein. To investigate the role of this gene in virus replication, a BHV-1 UL25 deletion mutant was constructed. Although the UL25 mutant synthesizes late viral proteins and viral DNA, it fails to produce virus progeny in cells that do not express the UL25 gene, demonstrating that the UL25 protein is essential for the replicative cycle of BHV-1.

Development of a multiplex RT-PCR to detect transcription of varicella-zoster virus encoded genes.

The reverse transcription polymerase chain reaction (RT-PCR) is used commonly to analyse transcription of genes. In the field of virology it is an extremely helpful method to analyse the transcriptional activity of both, DNA and RNA viruses. The standard RT-PCR allows an investigation of the activity of only one gene.