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1 VZV and HCMV mouse models were developed by subcutaneous
2 VZV causes varicella (chicken pox) and herpes zoster (sh
3 VZV encephalitis is associated with severe neurological
4 VZV glycoprotein B (gB) peptides assembled into fibrils
5 VZV immunization of pediatric solid organ transplant rec
6 VZV mutants with both an ITIM mutation and either alanin
7 VZV transcription during latency is restricted to the la
8 VZV vaccination also had no measurable effect on any of
9 VZV-conditioned supernatant contained increased interleu
10 VZV-infected qHA-sps produced intracellular amyloid and
11 VZV-infected qHA-sps, but not mock-infected qHA-sps, con
12 VZV-specific cell-mediated immunity is critical for the
13 VZV-specific cytotoxic T cell (VZV-CTL) and T follicular
14 zoster virus (VZV)-specific peak T helper 1 (VZV-Th1) responses to ZVL were independently predicted b
15 informatics analyses identified more than 20 VZV-encoded 20- to 24-nucleotide RNAs, some of which are
18 esults suggested that (i) Pompe cells lack a VZV trafficking pathway within M6PR-positive large endos
24 preclinical small-animal model for HCMV and VZV and, potentially, other human-restricted viruses.IMP
26 ions of congenital cytomegalovirus, HSV, and VZV with perinatal and maternal factors (sex, mother's e
28 intestine for specific cell type markers and VZV RNA demonstrated VZV-infected lymphocytes and neuron
30 and amyloid, was compared between mock- and VZV-infected quiescent primary human spinal astrocytes (
33 fully vaccinated against measles, mumps, and VZV, Bio-Rad MFI/Bion IFA positivity rates were 77.4%/93
34 Our study shows that VZV-specific PCs and VZV-specific CD4 memory T cells persist up to 20 years a
36 eronegative for measles, mumps, rubella, and VZV, respectively, and 165 (14%) were seronegative for a
37 ively immune to measles, mumps, rubella, and VZV, the Bio-Rad MFI was positive in 77.3, 85.4, 84.3, a
40 PE) cell line, ARPE-19, with cell-associated VZV and compared its response to that of the MeWo cell l
41 revent HZ; one is based on a live attenuated VZV strain (Zostavax), and the other is based on adjuvan
42 ere immunized with high-dose live attenuated VZV vaccine, and we assessed the expression on CD4+ T ce
45 These results suggest that IFN-gamma blocks VZV replication by inhibiting IE62 function in a cell li
46 These results suggest that IFN-gamma blocks VZV replication by inhibiting IE62 function in a cell li
58 ion was associated with concurrent decreased VZV-memory and CD8(+) effector responses, respectively,
60 c cell type markers and VZV RNA demonstrated VZV-infected lymphocytes and neurons in the gut wall and
68 r with host and other environmental factors, VZV infection may increase the toxic amyloid burden and
72 FN-gamma)-producing CD4 T cells specific for VZV glycoprotein E and all other structural and nonstruc
75 oscopy structure of native gB recovered from VZV-infected cells, in complex with a human monoclonal a
77 a42 were detected, yet only supernatant from VZV-infected cells induced amylin aggregation and, to a
78 oung adults had an increase in dual-function VZV-specific CD4(+) and CD8(+) T cell effectors defined
82 ler than those of other human herpesviruses, VZV has a similarly sized capsid, consisting of 955 majo
85 ore, given the prospect of developing an HIV/VZV chimeric vaccine, it is particularly important to de
90 simplex I/II or varicella zoster virus [HSV/VZV], blood stream infection [BSI], invasive fungal infe
91 ricella-zoster virus cell-mediated immunity (VZV-CMI) of adults >=70 years who received a second dose
97 t, older adults showed marginal increases in VZV-specific CD8(+)CD57(+) senescent T cells after vacci
99 tification of the role of the JNK pathway in VZV infection of neurons reveals potential avenues for t
100 echanisms by which IFN-gamma plays a role in VZV gene programming may be important in determining the
101 es (MAPKs) have been shown to play a role in VZV infection of nonneuronal cells, with distinct conseq
103 e that this M6PR pathway is most utilized in VZV infection and least utilized in HSV1 infection, with
107 RNA14 and VZVsncRNA9 decreased and increased VZV growth, respectively, while LNAA to three other VZVs
110 ive large endosomes and (ii) most infectious VZV particles in conventional cell substrates are transp
111 lasts or melanoma cells, multiple infectious VZV particles accumulated within large M6PR-positive lat
112 gonucleotides targeting VZVsncRNA to inhibit VZV replication strengthens the possibility that they ma
116 Wo cells, indicating that IFN-gamma inhibits VZV replication as well as IE62-mediated transactivation
117 wly infected cell nuclei, where it initiates VZV replication by transactivating viral immediate early
118 unctional observations provide insights into VZV assembly and pathogenesis and should help efforts to
119 f IFN-gamma completely reduced intracellular VZV yield in A549 lung epithelial cells, MRC-5 lung fibr
121 of virus with high titers, and for isolating VZV from clinical specimens.IMPORTANCE Varicella-zoster
122 us latency.IMPORTANCE Reactivation of latent VZV in humans can result in serious neurological complic
127 odies, extensive colocalization of the major VZV glycoprotein gE (known to contain M6P residues) and
129 onstrate that several VZVsncRNA can modulate VZV growth, including four VZVsncRNA (VZVsncRNA10, -11,
131 E and all other structural and nonstructural VZV proteins in both BM and blood (peripheral blood mono
134 Whole-exome sequencing (WES), analyses of VZV T-cell immunity, and pathogen recognition receptor f
135 omycin treatment led to impaired assembly of VZV capsids after primary envelopment/de-envelopment but
136 ings indicate the need for authentication of VZV by sequencing when the virus is propagated in tissue
137 become fatal, and although only few cases of VZV infection were detected, results from this study sug
142 light the critical role of IFN in control of VZV infections and suggest new approaches for treatment
144 VZV encephalitis, diagnosed by detection of VZV DNA in cerebrospinal fluid (CSF) by PCR and concomit
146 omly assigned (1:1) to receive four doses of VZV vaccine inactivated by gamma irradiation or placebo
147 interventional study, we offered 2 doses of VZV vaccine to all eligible and nonseroprotected childre
148 idence to our knowledge about the effects of VZV vaccination on human mucosal IA status and supports
149 srupted the site of secondary envelopment of VZV capsids by altering the pH of the trans-Golgi networ
150 clearly impacted cytoplasmic envelopment of VZV capsids, resulting in a dramatic increase of envelop
156 treatment, indicating that the inhibition of VZV replication is mediated by JAK/STAT1 signaling.
160 xpected deletion of a significant portion of VZV ORF 12 following propagation in cultured human fibro
167 tages compared to other cells for studies of VZV pathogenesis, for obtaining stocks of virus with hig
168 sembly compartments.IMPORTANCE This study of VZV assembly in the presence of bafilomycin A1 emphasize
169 ense to the latency-associated transcript of VZV can positively influence productive VZV infection.
170 anti-sncRNA-based therapies for treatment of VZV diseases.IMPORTANCE Varicella-zoster virus (VZV) cau
171 and suggest new approaches for treatment of VZV infection in patients with certain immune deficienci
173 investigated the effect of ORF7 deletion on VZV replication cycle at virus entry, genome replication
176 cted by the factors mentioned above, by peak VZV-Th1 responses to ZVL, and by the age of the vaccinee
180 re independently predicted by prevaccination VZV-Th1 responses, regulatory T cells (Treg), and PD1-ex
187 o-electron microscopy structures of purified VZV A-capsid and C-capsid, as well as of the DNA-contain
188 6 patients were randomly assigned to receive VZV vaccine inactivated by gamma irradiation (n=2637) or
191 sed exaggerated syncytium formation, reduced VZV titers (-1.5 log10), and smaller plaques than with t
195 hat of acyclovir, and an acyclovir-resistant VZV isolate was as sensitive to the effects of JNK inhib
196 ith age, but similar to other Th1 responses, VZV-CTL peak and baseline responses were independently c
200 es confer increased susceptibility to severe VZV disease in otherwise healthy children, providing evi
202 ZVIN elicited a statistically significant VZV-specific immune response approximately 28 days post-
204 developed an adult human skin model to study VZV and HCMV in culture and in vivo While VZV is known t
205 hat human neurons may be useful for studying VZV in vitro, for growing preparations of virus with hig
206 e, we showed in 15 healthy young adults that VZV-specific B and CD4 T cell responses are detectable i
207 se data strongly support the conclusion that VZV replication is modulated by multiple virally encoded
215 cluster (K894, K897, K898, and K900) in the VZV gBcyt was identified by sequence alignment to be con
216 analyses mapped to the repeat regions of the VZV genome, upstream of the predicted promoter of the im
217 tral location for most internal nodes of the VZV phylogeny, including the ancestor of clade 5 strains
218 ibodies targeting the N and C termini of the VZV SCP indicates that the hexon-capping SCP-the largest
221 ese results suggest that sncRNA antisense to VZV may regulate VZV growth, possibly by affecting VLT e
224 ut the cytokine and lymphocytic responses to VZV infection of RPE cells, thereby providing a useful p
227 ents displayed defective IFN production upon VZV infection and reduced control of VZV replication.
228 and during the first year after vaccination, VZV-CMI was significantly higher in reimmunized compared
229 tive titers (off label) against the VaccZyme VZV glycoprotein (VZVgp) low-level IgG kit (The Binding
230 The herpesviruses varicella-zoster virus (VZV) and human cytomegalovirus (HCMV) are endemic to hum
231 nd 2 (HSV-1, HSV-2), varicella-zoster virus (VZV) and human herpesvirus 8 (HHV-8) were not or rarely
232 ruses, most commonly varicella-zoster virus (VZV) and pseudorabies virus (PRV), may cause cranial ner
233 Infections with varicella-zoster virus (VZV) are associated with a range of clinical manifestati
234 ) and 2 (HSV-2), and varicella zoster virus (VZV) by weekly polymerase chain reaction in plasma.
237 diseases.IMPORTANCE Varicella-zoster virus (VZV) causes herpes zoster, a major health issue in the a
239 udied a patient with varicella-zoster virus (VZV) CNS vasculopathy and as part of the evaluation, tes
240 ort, we investigated varicella-zoster virus (VZV) egress in a cell line from a child with Pompe disea
242 euronal infection by varicella-zoster virus (VZV) have been challenging to study due to the relativel
243 IMPORTANCE Childhood varicella-zoster virus (VZV) immunization induces immune memory responses that p
245 ntibody responses to varicella-zoster virus (VZV) in vaccinated individuals, who produce lower antibo
246 nt primary wild-type varicella-zoster virus (VZV) infection, in whom chickenpox rash developed 2 days
250 62 (IE62) protein of varicella-zoster virus (VZV) is delivered to newly infected cell nuclei, where i
253 iant cell arteritis, varicella zoster virus (VZV) is seen in perineurial cells that surround adventit
256 osure to circulating varicella zoster virus (VZV) over the life span inhibits reactivation of VZV.
260 ty of an inactivated varicella zoster virus (VZV) vaccine for herpes zoster prevention in patients wi
263 arr virus (EBV), and varicella zoster virus (VZV) was determined in crewmembers and ground-based cont
264 L-10 and immunity to varicella zoster virus (VZV) were measured at baseline and after vaccination.
267 counterpart of human varicella-zoster virus (VZV), developed primary infection with viremia and rash,
268 ant alphaherpesvirus varicella-zoster virus (VZV), induce fusion of the virion envelope with cell mem
271 , we determined that varicella-zoster virus (VZV)-specific peak T helper 1 (VZV-Th1) responses to ZVL
276 work has shown that varicella-zoster virus (VZV; also called human herpesvirus 3 [HHV3]), the human
280 umps, rubella, and varicella-zoster viruses (VZV; MMRV) is a common condition of employment for healt
282 Blocking the PD1 pathway during ex vivo VZV restimulation increased the CD4(+) and CD8(+) prolif
284 mergency caesarean section deliveries, while VZV infection was associated with increased parity and b
285 dy VZV and HCMV in culture and in vivo While VZV is known to grow in skin, it was unknown whether ski
286 l of this research has been to determine why VZV, when grown in cultured cells, invariably is more ce
290 n electron microscopy, neurons infected with VZV produced fewer defective or incomplete viral particl
293 Our results indicate that patients with VZV encephalitis suffer from cognitive impairment long t
296 are nearly 100 times more permissive for WT VZV infection than very-early-passage human embryonic lu
297 em cells (hESC) and cell-free wild-type (WT) VZV, we demonstrated that neurons are nearly 100 times m
298 ed in 22 of 1328 (6.7 per 1000 person-years) VZV vaccine recipients and in 61 of 1350 (18.5 per 1000
300 yellow-fever or varicella-zoster virus (YFV/VZV) vaccines was more suspended, with early IFN-associa