نتایج جستجو برای: zoster virus vzv

تعداد نتایج: 406069  

Journal: :The Journal of general virology 2005
Peter G E Kennedy Esther Grinfeld Marie Craigon Klemens Vierlinger Douglas Roy Thorsten Forster Peter Ghazal

Varicella-zoster virus (VZV) is a human herpes virus that causes varicella as a primary infection and herpes zoster following reactivation of the virus from a latent state in trigeminal and spinal ganglia. In order to study the global pattern of VZV gene transcription, VZV microarrays using 75-base oligomers to 71 VZV open reading frames (ORFs) were designed and validated. The long-oligonucleot...

Journal: :Journal of virology 2014
Xueqiao Liu Jeffrey I Cohen

Programmed cell death (apoptosis) is an important host defense mechanism against intracellular pathogens, such as viruses. Accordingly, viruses have evolved multiple mechanisms to modulate apoptosis to enhance replication. Varicella-zoster virus (VZV) induces apoptosis in human fibroblasts and melanoma cells. We found that VZV triggered the phosphorylation of the proapoptotic proteins Bim and B...

2013
Kristen Haberthur Ilhem Messaoudi

Primary infection with varicella zoster virus (VZV) results in varicella (chickenpox) followed by the establishment of latency in sensory ganglia. Declining T cell immunity due to aging or immune suppressive treatments can lead to VZV reactivation and the development of herpes zoster (HZ, shingles). HZ is often associated with significant morbidity and occasionally mortality in elderly and immu...

Journal: :Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2001
K Schmader

Herpes zoster (HZ) strikes millions of older adults annually worldwide and disables a substantial number of them via postherpetic neuralgia (PHN). Key age-related clinical, epidemiological, and treatment features of zoster and PHN are reviewed. HZ is caused by renewed replication and spread of varicella-zoster virus (VZV) in sensory ganglia and afferent peripheral nerves in the setting of age-r...

2007
Anita E Heywood Kristine K Macartney Peter B McIntyre

On 16 and 17 November 2006, the National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases (NCIRS) hosted a workshop on varicella-zoster virus (VZV) disease. The workshop was aimed at presenting the latest information on the clinical, epidemiological, and diagnostic aspects of both primary varicella (‘chickenpox’) and herpes zoster (HZ or ‘shingles’) both in Aust...

2015
Charles Grose Erin M Buckingham Wallen Jackson John E Carpenter

Autophagy has been intensively studied in herpes simplex virus type 1 (HSV-1), a human alphaherpesvirus. The HSV-1 genome encodes a well-known neurovirulence protein called ICP34.5. When the gene encoding this protein is deleted from the genome, the virus is markedly less virulent when injected into the brains of animal models. Subsequent characterization of ICP34.5 established that the neurovi...

Journal: :Viruses 2021

Varicella-Zoster virus (VZV) is a human herpesvirus that causes varicella (chickenpox) as primary infection, and, following variable period of ganglionic latency in neurons, it reactivates to cause herpes zoster (shingles). An analysis VZV infection cultures neural cells, particular when these have been obtained from induced pluripotent stem cells (iPSCs) or consisting highly purified neuronal ...

Journal: :Arthritis and rheumatism 1993
I Amoura A M Fillet J M Huraux P Bourgeois

Only a few cases of herpes zoster-associated arthritis have been reported to date (1-3). This form of arthritis is presumed to be viral in origin. Isolation of varicella zoster virus (VZV) by culture from synovial fluid has not been previously documented. VZV infection of the joint space associated with acute arthritis has been evidenced only once, by the finding of VZV antigen in the joint flu...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1986
E A Montalvo C Grose

Varicella zoster virus glycoprotein I (VZV gpI; Mr 98,000) was phosphorylated in virus-infected human cell monolayers, while two other major VZV glycoproteins (gpII and gpIII) were not similarly modified. Phosphorylation of VZV gpI was not blocked by inhibitors of glycosylation, nor were the phosphoryl groups enzymatically removed by endoglycosidases. Phosphoamino acid analysis revealed the pre...

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