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Showing 1-21 of 21 results for "mab8612" within Papers
Shirley E Braspenning et al.
Viruses, 13(11) (2021-11-28)
Primary varicella-zoster virus (VZV) infection leads to varicella and the establishment of lifelong latency in sensory ganglion neurons. Reactivation of latent VZV causes herpes zoster, which is frequently associated with chronic pain. Latent viral gene expression is restricted to the
Yuri Ishino et al.
BMC nephrology, 24(1), 164-164 (2023-06-09)
Visceral disseminated varicella zoster virus (VZV) infection is a rare but life-threatening complication in immunosuppressed patients. Herein, we report a survival case of visceral disseminated VZV infection in a patient with systemic lupus erythematosus (SLE). A 37-year-old woman was diagnosed
Apparent expression of varicella-zoster virus proteins in latency resulting from reactivity of murine and rabbit antibodies with human blood group a determinants in sensory neurons.
Zerboni, L; Sobel, RA; Lai, M; Triglia, R; Steain, M; Abendroth, A; Arvin, A
Journal of virology null
Identification of an important immunological difference between virulent varicella-zoster virus and its avirulent vaccine: viral disruption of dendritic cell instruction.
Cindy Gutzeit,Martin J Raftery,Matthias Peiser,Karsten B Tischer,Martina Ulrich et al.
Journal of immunology (Baltimore, Md. : 1950) (1950)
Varicella-zoster virus (VZV) open reading frame 10 protein, the homolog of the essential herpes simplex virus protein VP16, is dispensable for VZV replication in vitro.
Cohen, J I and Seidel, K
Journal of virology, 68, 7850-7858 (1994)
Deletion of the varicella-zoster virus large subunit of ribonucleotide reductase impairs growth of virus in vitro.
Heineman, T C and Cohen, J I
Journal of virology, 68, 3317-3323 (1994)
Mutagenesis of varicella-zoster virus glycoprotein I (gI) identifies a cysteine residue critical for gE/gI heterodimer formation, gI structure, and virulence in skin cells.
Stefan L Oliver,Marvin H Sommer,Mike Reichelt,Jaya Rajamani,Leonssia Vlaycheva-Beisheim et al.
Journal of virology null
Robert M Verdijk et al.
The Journal of infectious diseases, 223(1), 109-112 (2020-09-10)
To test the hypothesis that varicella-zoster virus (VZV) infection contributes to temporal arteritis pathogenesis, comprehensive in situ analysis was performed on temporal artery biopsies of 38 anterior ischemic optic neuropathy (AION) patients, including 14 (37%) with giant cell arteritis. Biopsies
Shirley E Braspenning et al.
mBio, 11(5) (2020-10-08)
Varicella-zoster virus (VZV), a double-stranded DNA virus, causes varicella, establishes lifelong latency in ganglionic neurons, and reactivates later in life to cause herpes zoster, commonly associated with chronic pain. The VZV genome is densely packed and produces multitudes of overlapping
Identification and functional characterization of the Varicella zoster virus ORF11 gene product.
Xibing Che,Stefan L Oliver,Marvin H Sommer,Jaya Rajamani,Mike Reichelt,Ann M Arvin
Virology null
Development of recombinant varicella-zoster viruses expressing luciferase fusion proteins for live in vivo imaging in human skin and dorsal root ganglia xenografts.
Stefan L Oliver, Leigh Zerboni, Marvin Sommer, Jaya Rajamani, Ann M Arvin et al.
Journal of Virological Methods null
Edward Yang et al.
PLoS pathogens, 10(5), e1004173-e1004173 (2014-05-31)
The conserved herpesvirus fusion complex consists of glycoproteins gB, gH, and gL which is critical for virion envelope fusion with the cell membrane during entry. For Varicella Zoster Virus (VZV), the complex is necessary for cell-cell fusion and presumed to
Hirobumi Saitoh et al.
Internal medicine (Tokyo, Japan), 52(15), 1727-1730 (2013-08-02)
Disseminated visceral varicella-zoster virus (VZV) infection rarely occurs in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT). To date, only a few cases of isolated VZV-induced fulminant hepatitis following allo-HSCT have been reported. We herein describe the case of a
Daichi Fujimoto et al.
Medical molecular morphology, 55(4), 316-322 (2022-06-19)
Patients with SARS-CoV-2 infection and with severe COVID-19 often have multiple coinfections, and their treatment is challenging. Here, we performed cytology analysis on sputum samples from two patients with severe COVID-19. The specimens were prepared using the rubbing method and
Melissa A Visalli et al.
Journal of virology, 88(14), 7973-7986 (2014-05-09)
The varicella-zoster virus (VZV) open reading frame 54 (ORF54) gene encodes an 87-kDa monomer that oligomerizes to form the VZV portal protein, pORF54. pORF54 was hypothesized to perform a function similar to that of a previously described herpes simplex virus
Daniel P Depledge et al.
Nature communications, 9(1), 1167-1167 (2018-03-23)
Varicella-zoster virus (VZV), an alphaherpesvirus, establishes lifelong latent infection in the neurons of >90% humans worldwide, reactivating in one-third to cause shingles, debilitating pain and stroke. How VZV maintains latency remains unclear. Here, using ultra-deep virus-enriched RNA sequencing of latently
Ryo Takahashi et al.
Journal of immunology (Baltimore, Md. : 1950), 192(3), 969-978 (2014-01-01)
It remains unknown why the occurrence of eczema herpeticum (EH) caused by an extensive disseminated cutaneous infection with HSV-1 or HSV-2 is associated with the exacerbation of atopic dermatitis lesions after withdrawal of treatment. Although regulatory T cells (Tregs) limit
Varicella-zoster virus ORF12 protein activates the phosphatidylinositol 3-kinase/Akt pathway to regulate cell cycle progression.
Liu, X; Cohen, JI
Journal of virology null
Shuzhao Li et al.
Cell, 169(5), 862-877 (2017-05-16)
Herpes zoster (shingles) causes significant morbidity in immune compromised hosts and older adults. Whereas a vaccine is available for prevention of shingles, its efficacy declines with age. To help to understand the mechanisms driving vaccinal responses, we constructed a multiscale
Kerry J Laing et al.
Nature communications, 13(1), 6957-6957 (2022-11-15)
Herpes zoster is a localized skin infection caused by reactivation of latent varicella-zoster virus. Tissue-resident T cells likely control skin infections. Zoster provides a unique opportunity to determine if focal reinfection of human skin boosts local or disseminated antigen-specific tissue-resident
Stefan L Oliver et al.
Journal of virology, 83(15), 7495-7506 (2009-05-29)
Glycoprotein B (gB), the most conserved protein in the family Herpesviridae, is essential for the fusion of viral and cellular membranes. Information about varicella-zoster virus (VZV) gB is limited, but homology modeling showed that the structure of VZV gB was
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