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.

Testing virucidal activity in Germany: an update.

Several chemical disinfectants have been tested in a quantitative suspension test for virucidal activity as per the test method devised by the German Society for Control of Viral Diseases (DVV) and the former German Federal Health Office (BGA, now the Robert Koch-Institute, RKI) drafted in 1982. The introduction of the term "limited virucidal activity" (effective against enveloped viruses) in addition to the existing term "virucidal activity" (effective against non-enveloped and enveloped viruses) by the Robert Koch Institute has led to enormous expansion of these tests. However, there are no definitions to determine when a disinfectant with virucidal activity as apposed to a disinfectant with limited virucidal activity is to be used.

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.

A survey to detect subclinical polyomavirus infections of captive psittacine birds in Germany.

Infections of avian polyomavirus (APV) are known to cause fatal disease in a wide range of psittacine and non-psittacine birds. Here, we present a survey to investigate the existence of subpopulation of persistent or subclinically infected parrots inside the population of captive psittacine birds in Germany. DNA was isolated from feathers of 85 symptom-free birds from 20 different genera (all psittaciformes) taken from 30 different breeders from all over Germany.

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.

Psittacine beak and feather disease: a first survey of the distribution of beak and feather disease virus inside the population of captive psittacine birds in Germany.

Psittacine beak and feather disease (PBFD) is the most common viral disease of wild and captive psittacine birds. Here, we designed the first survey to investigate the existence of subclinical infections and the distribution of the causative agent named beak and feather disease virus (BFDV) inside the population of captive psittacine birds in Germany. DNA was isolated from feathers of 146 symptom-free birds from 19 different genera (all psittaformes) taken from 32 independent breeders from all over Germany.

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.

The varicella-zoster virus induces apoptosis in vitro in subpopulations of primary human peripheral blood mononuclear cells.

Varicella-zoster virus (VZV), a member of Herpesviridae, subfamily alpha-Herpesvirinae, is pathogenic exclusively in the human. Chickenpox is the result of primary infection of VZV. During the viremic stage, VZV infects peripheral blood mononuclear cells (PBMC) and spreads to the periphery.

Infectibility of separated peripheral blood mononuclear cell subpopulations by varicella-zoster virus (VZV).

Varicella zoster-virus (VZV) is a humanpathogenic alpha-Herpesvirus that causes chickenpox after primary infection. The virus spreads by aerosol or direct contact with infectious vesical fluids, it enters the body via the respiratory tract. In a first viremic stage it replicates in local lymph nodes, followed by a secondary viremic stage.

Analyses of the transcriptional pattern of glycoproteins E and I of Varicella-zoster virus and evidence for a monocistronic transcription.

Glycoproteins I and E of the Varicella-zoster virus, encoded by the neighbouring open reading frames 67 and 68, are transcribed into several transcript species that differ in size. From gI, three transcripts of 1.65, 2.

Reciprocal effects of varicella-zoster virus (VZV) and AP1: activation of jun, fos and ATF-2 after VZV infection and their importance for the regulation of viral genes.

Varicella-zoster virus, an alpha-herpesvirus that is pathogenic for man, encodes its own transcription activators, but ubiquitous cellular transcription factors are of great importance, too. Performing quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) we found an increase of transcription of AP1 components jun, fos and of ATF-2 at different times post infection (p.i.

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.

Clinical and subclinical reactivation of genital herpes virus.

Reactivations of herpes simplex virus (HSV) either symptomatically (recrudescence) or without symptoms (recurrence) are well documented. As an asymptomatic reactivation may contribute to transmitting HSV to potential acceptors the frequency of reactivations should be evaluated. In order to evaluate the frequency of HSV-2 reactivation 173 genital swabs of a group of women chosen at random were analyzed by nested PCR.

Varicella-zoster virus (VZV) mediates a delayed host shutoff independent of open reading frame (ORF) 17 expression.

Varicella-zoster virus (VZV) open reading frame 17 (ORF 17) is the gene corresponding to Herpes simplex-virus (HSV) UL41. The UL41 gene encodes the virion host shutoff factor (vhs), a RNase that has been the object of detailed studies. In contrast to HSV, knowledge about VZV mediated shutoff effects and the role of ORF 17 is poor.