Disease relevance of Herpesvirus 3, Human

• Immunofluorescence for herpes simplex virus, varicella-zoster virus, and cytomegalovirus gave negative results in all cases, but 19 of 20 specimens showed intense nuclear staining in epithelial cells for the viral capsid antigen of Epstein-Barr virus (EBV) [1].
• Acyclovir has been the mainstay for treating severe varicella-zoster virus infections; however, newer antiviral agents, including valacyclovir and famciclovir, have expanded therapeutic options for treating adults with herpes zoster [2].
• Acyclovir resistance is usually seen in patients with large, untreated, ulcerative lesions of herpes simplex virus and in patients with chronic, verrucous lesions of varicella-zoster virus [3].
• The product of varicella-zoster virus gene 62 (VZV 140k) is the functional counterpart of the major transcriptional regulatory protein of herpes simplex virus type 1 (HSV-1), ICP4 [4].
• Amino acid substitution mutations were introduced into five regions of the UL52 gene that are highly conserved among HSV-1 and the related herpesviruses equine herpesvirus 1, human cytomegalovirus, Epstein-Barr virus, and varicella-zoster virus [5].

High impact information on Herpesvirus 3, Human

• Acyclovir was well tolerated, and there was no significant difference between groups in the titers of antibodies against varicella-zoster virus [6].
• Treatment of varicella-zoster virus infection in severely immunocompromised patients. A randomized comparison of acyclovir and vidarabine [7].
• These stored samples were tested in parallel by enzyme-linked immunosorbent assay, latex agglutination, and Western blot for IgG antibodies to varicella-zoster virus (VZV) [8].
• Carriers of a 32 bp deletion (Delta32) allele of the CC chemokine receptor 5 (CCR5) gene are reported to be more likely to lack antibodies to varicella-zoster virus than CCR5 wild-type individuals [9].
• We have studied the intracellular trafficking of the envelope glycoprotein I (gpI) of the varicella-zoster virus, a human herpes virus whose assembly is believed to occur in the trans-Golgi network (TGN) and/or in endocytic compartments [10].

Chemical compound and disease context of Herpesvirus 3, Human

• PATIENTS: Five patients with AIDS who were infected with thymidine-kinase-deficient or -altered strains of varicella-zoster virus [11].
• The varicella-zoster virus (VZV) genes ORF47 and ORF66 are predicted to encode serine/threonine protein kinases, which are homologs of herpes simplex virus 1 (HSV-1) UL13, and US3 [12].
• 2-Acetylpyridine 5-[(dimethylamino)thiocarbonyl]thiocarbonohydrazone (A1110U) was found to be a potent inactivator of the ribonucleotide reductases (EC 1.17.4.1) encoded by herpes simplex virus types 1 and 2 and by varicella-zoster virus and to be a weaker inactivator of human ribonucleotide reductase [13].
• Gene activation by Varicella-zoster virus IE4 protein requires its dimerization and involves both the arginine-rich sequence, the central part, and the carboxyl-terminal cysteine-rich region [14].
• Disseminated varicella-zoster virus infection with the syndrome of inappropriate antidiuretic hormone [15].

Biological context of Herpesvirus 3, Human

• Characterization of Varicella-Zoster virus glycoprotein K (open reading frame 5) and its role in virus growth [16].
• Identification of the phosphorylation sequence in the cytoplasmic tail of the varicella-zoster virus Fc receptor glycoprotein gpI [17].
• The accumulation of recent data concerning the reactivity of monoclonal antibodies with particular varicella-zoster virus (VZV) glycoproteins and the mapping of several of their respective genes on the VZV genome has led to a unified nomenclature for the glycoprotein genes of VZV and their mature glycosylated products [18].
• Restriction fragment length polymorphism of polymerase chain reaction products from vaccine and wild-type varicella-zoster virus isolates [19].
• Endocytosis and recycling of varicella-zoster virus Fc receptor glycoprotein gE: internalization mediated by a YXXL motif in the cytoplasmic tail [20].

Anatomical context of Herpesvirus 3, Human

• Noninfected and varicella-zoster virus (VZV)-infected human foreskin fibroblasts were examined for thymidine kinase activity [21].
• Varicella-zoster virus ORF47 protein kinase, which is required for replication in human T cells, and ORF66 protein kinase, which is expressed during latency, are dispensable for establishment of latency [22].
• Quantitation of latent varicella-zoster virus DNA in human trigeminal ganglia by polymerase chain reaction [23].
• Role of cytoplasmic vacuoles in varicella-zoster virus glycoprotein trafficking and virion envelopment [24].
• Polymerase chain reaction detection and clinical significance of varicella-zoster virus in cerebrospinal fluid from human immunodeficiency virus-infected patients [25].

Gene context of Herpesvirus 3, Human

• Exon 2 encodes a putative circ-encoded protein with homology to the varicella-zoster virus open reading frame 2 and equine herpesvirus 1 open reading frame 3 products [26].
• Roscovitine, a cyclin-dependent kinase inhibitor, prevents replication of varicella-zoster virus [27].
• We demonstrated that varicella-zoster virus (VZV) activates inflammatory cytokine responses via TLR2 [28].
• Varicella-zoster virus Fc receptor component gI is phosphorylated on its endodomain by a cyclin-dependent kinase [29].
• The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter [30].

Analytical, diagnostic and therapeutic context of Herpesvirus 3, Human

• Glycoprotein gp118 of varicella-zoster virus: purification by serial affinity chromatography [31].
• For examination of the clinical efficacy of FIAC, a randomized, double-blind study of FIAC versus adenine arabinoside (ara-A) was conducted in 34 immunosuppressed individuals with varicella-zoster virus infections [32].
• Antigen detection by a direct immunofluorescence assay with a fluorescein isothiocyanate-labelled monoclonal antibody, virus isolation, and serologic methods (in-house varicella-zoster virus [VZV] immunoglobulin G [IgG] and IgM enzyme-linked immunosorbent assays and the commercial Enzygnost assay) were compared [33].
• An immunoglobulin M response to varicella-zoster virus was detected in 70% of zoster patients by solid-phase radioimmunoassay, in 52% by indirect immunofluorescence, in 48% by neutralization on sucrose density gradient fractions, and in 27% by an antibody class capture enzyme immunoassay [34].
• A fluorescent antibody to membrane antigen assay was used for determination of the antibody to varicella-zoster virus, and a nested polymerase chain reaction method was used for detection of viremia [35].

References