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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
16      This pattern indicates that the clade 5 VZV strains do not represent recent introductions from A
17          To corroborate in vitro findings, a VZV-infected TA was examined.
18 esults suggested that (i) Pompe cells lack a VZV trafficking pathway within M6PR-positive large endos
19                                    We used a VZV antigen challenge system in the skin to investigate
20 10, increasing NR4A1 expression and allowing VZV replication and propagation.
21 V (63.8%), measles (1.4%), mumps (6.6%), and VZV (3.8%).
22 ntibody-secreting plasma cells in the BM and VZV-specific CD4 T cells in BM and blood.
23 DNA concentrations, particularly for EBV and VZV.
24  preclinical small-animal model for HCMV and VZV and, potentially, other human-restricted viruses.IMP
25 sor of acyclovir in the treatment of HSV and VZV infections.
26 ions of congenital cytomegalovirus, HSV, and VZV with perinatal and maternal factors (sex, mother's e
27 her for congenital cytomegalovirus, HSV, and VZV, whereas it was lower for rubella.
28 intestine for specific cell type markers and VZV RNA demonstrated VZV-infected lymphocytes and neuron
29                                    Mock- and VZV-infected primary human perineurial cells (HPNCs) wer
30  and amyloid, was compared between mock- and VZV-infected quiescent primary human spinal astrocytes (
31  presumptively immune to measles, mumps, and VZV (a rubella IFA was unavailable).
32  viruses, including HAV, measles, mumps, and VZV (P < 0.05 for all).
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
35   Cognitive impairment has been reported and VZV has been associated with dementia.
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
38                                         Anti-VZV plasma antibody titers correlated positively with th
39 use the reactivation efficiently boosts anti-VZV immunity.
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
43 esses leading to hyperfusion that attenuates VZV infection.
44 cer vectors based on the currently available VZV vaccine.
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
47 et for intervention of neuropathy induced by VZV.
48                               In rare cases, VZV can give rise to life-threatening disease in otherwi
49               VZV-specific cytotoxic T cell (VZV-CTL) and T follicular helper responses to ZVL did no
50 hy young adults (n = 15) following childhood VZV immunization.
51      In the United States, routine childhood VZV vaccination was introduced only 2 decades ago.
52       These findings indicate that childhood VZV vaccination can elicit long-lived immune memory resp
53        These findings suggest that childhood VZV vaccination induces long-lived immunity.
54                             Although common, VZV infection can be life-threatening, particularly in t
55 This may underlie their inability to contain VZV reactivation and prevent the development of HZ.
56                                 In contrast, VZV is highly infectious in vivo by airborne transmissio
57 bal gene activation at the site of cutaneous VZV antigen challenge compared with young subjects.
58 ion was associated with concurrent decreased VZV-memory and CD8(+) effector responses, respectively,
59  of PD1 and CTLA4 as modulators of decreased VZV-Th1 responses in the study participants.
60 c cell type markers and VZV RNA demonstrated VZV-infected lymphocytes and neurons in the gut wall and
61                         Notably, we detected VZV- and HCMV-infected cells in the contralateral, unino
62 tutively secrete antibodies, and we detected VZV-specific PCs in the BM of all subjects.
63 cessfully grows in adult human skin, as does VZV.
64                  We hypothesized that during VZV reactivation from ganglia, virus travels transaxonal
65 us enzyme-linked immunosorbent assay (ELISA) VZV IgG assay (Zeus Diagnostics, Branchburg, NJ).
66 o the miRNA candidate significantly enhanced VZV plaque growth rates.
67                          We show that extant VZV strains most likely originated in Europe and not in
68 r with host and other environmental factors, VZV infection may increase the toxic amyloid burden and
69 .6 (14.6-21.1) for HSV, 32.6 (28.4-37.2) for VZV, and 0.15 (0.0-0.8) for rubella.
70            gBcyt regulation is necessary for VZV pathogenesis, as the hyperfusogenic mutant gB[Y881F]
71 t, and widespread infection was observed for VZV and HCMV.
72 FN-gamma)-producing CD4 T cells specific for VZV glycoprotein E and all other structural and nonstruc
73                Neurons are major targets for VZV in vivo; in neurons, the virus can establish latency
74                                    Cell-free VZV has been difficult to obtain, both for in vitro stud
75 oscopy structure of native gB recovered from VZV-infected cells, in complex with a human monoclonal a
76                           IL-6 secreted from VZV-infected HPNCs facilitated changes in E- and N-cadhe
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
79                                 Furthermore, VZV reactivation correlates with a decline in IFN-gamma-
80      In the haematological malignancy group, VZV vaccine was well tolerated and estimated vaccine eff
81                                      Healthy VZV-seropositive Kenyan women (n = 44) were immunized wi
82 ler than those of other human herpesviruses, VZV has a similarly sized capsid, consisting of 955 majo
83                         This process hinders VZV and is regulated by a viral glycoprotein, gB.
84                                Historically, VZV is among the most genetically stable herpesviruses,
85 ore, given the prospect of developing an HIV/VZV chimeric vaccine, it is particularly important to de
86                                          How VZV establishes, maintains and reactivates from latency
87           The findings further elucidate how VZV self-regulates multinuclear cell formation and may p
88 l compounds active against DNA viruses (HSV, VZV, CMV, HBV) and retroviruses (HIV).
89 veloped the composite outcome (61 CMV, 3 HSV/VZV, 19 BSI, 10 IFI, 8 deaths).
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
92                        Although immunogenic, VZV vaccination did not result in significant difference
93                                           In VZV-infected HPNCs, claudin-1 redistributed to the nucle
94                                           In VZV-infected skin, kallikrein 6 and the ubiquitin ligase
95               In conclusion, the increase in VZV-CMI generated by reimmunization with ZVL is at least
96                               An increase in VZV-stimulated CD4(+)CD69(+)CD57(+)PD1(+) and CD8(+)CD69
97 t, older adults showed marginal increases in VZV-specific CD8(+)CD57(+) senescent T cells after vacci
98  MAPK, the c-Jun N-terminal kinase (JNK), in VZV lytic infection and reactivation.
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
102 adherin gained, with similar changes seen in VZV-infected perineurial cells in a TA.
103 e that this M6PR pathway is most utilized in VZV infection and least utilized in HSV1 infection, with
104 ho received at least one dose of inactivated VZV vaccine or placebo and had follow-up data.
105 ho received at least one dose of inactivated VZV vaccine or placebo).
106                              The inactivated VZV vaccine was well tolerated and efficacious for herpe
107 RNA14 and VZVsncRNA9 decreased and increased VZV growth, respectively, while LNAA to three other VZVs
108 deno-associated virus consistently increased VZV spread and progeny titers.
109 nterferon response factor 1 (IRF1) increased VZV replication.
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
113                          IFN-gamma inhibited VZV gene expression after the immediate early stage of i
114 howed that IFN-gamma significantly inhibited VZV replication in a cell line-dependent manner.
115             IFN-beta significantly inhibited VZV replication in both ARPE-19 and MeWo cells.
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
120 of erythema and induration after intradermal VZV antigen injection.
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
123  melanoma cells infected with wild-type-like VZV or hyperfusogenic mutants.
124                                          Low VZV-antibody concentration (<=400 UI/L) after the first
125 atment from 48 to 72 h postinfection lowered VZV titers substantially (P <= 0.008).
126 lved in the transition from latency to lytic VZV infection.
127 odies, extensive colocalization of the major VZV glycoprotein gE (known to contain M6P residues) and
128 tional units (IU)/ml (EBV) to 661 copies/ml (VZV).
129 onstrate that several VZVsncRNA can modulate VZV growth, including four VZVsncRNA (VZVsncRNA10, -11,
130 LT) and RNA 63 (encoding ORF63) in naturally VZV-infected human trigeminal ganglia (TG).
131 E and all other structural and nonstructural VZV proteins in both BM and blood (peripheral blood mono
132                                       Normal VZV-specific T-cell immunity and antibody response were
133                         The low abundance of VZV nucleic acids in human neurons has hindered an under
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
138              Consequently, if circulation of VZV is suppressed by introduction of chickenpox vaccinat
139 nserved between viruses from three clades of VZV.
140 nce for the definition and classification of VZV clades.
141 vealing an additional layer of complexity of VZV regulation of lytic infections.
142 light the critical role of IFN in control of VZV infections and suggest new approaches for treatment
143 on upon VZV infection and reduced control of VZV replication.
144  VZV encephalitis, diagnosed by detection of VZV DNA in cerebrospinal fluid (CSF) by PCR and concomit
145               The geographic distribution of VZV clades was taken as evidence that VZV migrated out o
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
151 IA status and supports further evaluation of VZV as a potential vector for an HIV vaccine.
152                            The expression of VZV IE62 and ORF63 suppressed by IFN-gamma was restored
153                             The frequency of VZV-specific IFN-gamma-producing CD4 T cells was signifi
154 mechanisms underlying the immunopathology of VZV-associated posterior uveitis.
155 rticularly important to define the impact of VZV vaccination on IA.
156 treatment, indicating that the inhibition of VZV replication is mediated by JAK/STAT1 signaling.
157 ers correlated positively with the number of VZV-specific BM PCs.
158                               Persistence of VZV-Th1 1 year after vaccination was independently predi
159 the specificity, magnitude, and phenotype of VZV-specific T cells.
160 xpected deletion of a significant portion of VZV ORF 12 following propagation in cultured human fibro
161            Here, we analyzed the quantity of VZV-specific plasma cells (PCs) and CD4 T cells in the b
162  over the life span inhibits reactivation of VZV.
163 ted in a marked reduction in reactivation of VZV.
164 ic flux is required for higher recoveries of VZV infectivity.
165 ant in determining the tissue restriction of VZV.
166  of autophagy in human skin, a major site of VZV assembly.
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
172  the marketed compounds for the treatment of VZV infections (i.e., herpes zoster).
173  investigated the effect of ORF7 deletion on VZV replication cycle at virus entry, genome replication
174                                 At least one VZV sncRNA was expressed in productive infection of neur
175                   Supportive data from other VZV, PRV, and HSV1 laboratories about evidence for two e
176 cted by the factors mentioned above, by peak VZV-Th1 responses to ZVL, and by the age of the vaccinee
177                 We used TB40/E HCMV and POka VZV strains to evaluate virus tropism in skin organ cult
178 pients developed symptoms and had a positive VZV PCR.
179 E-19 retinal epithelial cells at 4 days post-VZV infection.
180 re independently predicted by prevaccination VZV-Th1 responses, regulatory T cells (Treg), and PD1-ex
181                                  Previously, VZV and HCMV models used fetal tissue; here, we develope
182 emory responses that protect against primary VZV infection, chicken pox.
183 a potent cytokine produced following primary VZV infection.
184 ive YFV-vaccine recipients but not in primed VZV-vaccine recipients.
185 t of VZV can positively influence productive VZV infection.
186                  The influence on productive VZV growth and spread was assessed in epithelial cells t
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
189 ject was that inhibitors of autophagy reduce VZV infectivity.
190         Preventing KRT10 degradation reduced VZV propagation in culture and prevented epidermal disru
191 sed exaggerated syncytium formation, reduced VZV titers (-1.5 log10), and smaller plaques than with t
192           Ectopic expression of IRF1 reduced VZV yields 4,000-fold in MRC-5 and ARPE-19 cells but 3-f
193 st that sncRNA antisense to VZV may regulate VZV growth, possibly by affecting VLT expression.
194 d this study demonstrates the first reported VZV-encoded sncRNAs.
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
197                                      Routine VZV vaccination started only 2 decades ago, and thus, th
198  of JNK inhibition as an acyclovir-sensitive VZV isolate in neurons.
199            We report 4 cases of acute severe VZV infection affecting the central nervous system or th
200 es confer increased susceptibility to severe VZV disease in otherwise healthy children, providing evi
201                                  Significant VZV-specific T-cell responses followed vaccination only
202    ZVIN elicited a statistically significant VZV-specific immune response approximately 28 days post-
203                                      In SOC, VZV infected the epidermis and HCMV infected the dermis.
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
208 ion of VZV clades was taken as evidence that VZV migrated out of Africa with human populations.
209         Collectively, our findings show that VZV expresses a unique set of VLT-ORF63 transcripts, pot
210                                 We show that VZV grows to much higher titers in human neurons than in
211                We have previously shown that VZV induces levels of autophagy far above the basal leve
212                         Our study shows that VZV-specific PCs and VZV-specific CD4 memory T cells per
213                                          The VZV capsid has high thermal stability, although with rel
214 e infected Pompe cells and then assessed the VZV infectious cycle.
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
219                                         This VZV study also complemented prior herpes simplex virus 1
220                                        Thus, VZV may not necessarily have a higher particle-to-PFU ra
221 ese results suggest that sncRNA antisense to VZV may regulate VZV growth, possibly by affecting VLT e
222 amyloid fibrils that may be due, in part, to VZV gB peptides.
223          In contrast, cutaneous responses to VZV antigen challenge were increased significantly in th
224 ut the cytokine and lymphocytic responses to VZV infection of RPE cells, thereby providing a useful p
225                                   Similar to VZV in humans, SVV causes varicella in monkeys, establis
226                     Therefore, understanding VZV-keratinocyte interactions is important to find new t
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.
235 -restricted pathogen varicella-zoster virus (VZV) causes chickenpox and shingles.
236 specimens.IMPORTANCE Varicella-zoster virus (VZV) causes chickenpox and shingles.
237  diseases.IMPORTANCE Varicella-zoster virus (VZV) causes herpes zoster, a major health issue in the a
238                      Varicella-zoster virus (VZV) characteristically forms multinucleated cells, or s
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
241                      Varicella-zoster virus (VZV) establishes lifelong neuronal latency in most human
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
244 mplex virus (HSV) or varicella zoster virus (VZV) in 79% to 100% of cases of suspected ARN.
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
247                      Varicella-zoster virus (VZV) is a medically important human herpesvirus that cau
248                      Varicella zoster virus (VZV) is a skin-tropic virus that infects epidermal kerat
249                      Varicella-zoster virus (VZV) is an alphaherpesvirus that lacks the herpesviral n
250 62 (IE62) protein of varicella-zoster virus (VZV) is delivered to newly infected cell nuclei, where i
251                      Varicella-zoster virus (VZV) is highly cell associated when grown in culture and
252                      Varicella-zoster virus (VZV) is one of the most common agents causing viral infe
253 iant cell arteritis, varicella zoster virus (VZV) is seen in perineurial cells that surround adventit
254                      Varicella zoster virus (VZV) is the causative agent of chickenpox and shingles.
255                      Varicella-zoster virus (VZV) is under consideration as a promising recombinant v
256 osure to circulating varicella zoster virus (VZV) over the life span inhibits reactivation of VZV.
257  a characteristic of varicella-zoster virus (VZV) pathology in skin and sensory ganglia.
258                      Varicella zoster virus (VZV) typically causes chickenpox upon primary infection.
259                      Varicella-zoster virus (VZV) vaccine appears to be safe and immunogenic in pedia
260 ty of an inactivated varicella zoster virus (VZV) vaccine for herpes zoster prevention in patients wi
261  the live-attenuated varicella-zoster virus (VZV) vaccine induces protective immune responses.
262  the live-attenuated varicella-zoster virus (VZV) vaccine.
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.
265 .g. HSV-1, HSV-2 and varicella-zoster virus (VZV)).
266 simplex virus (HSV), varicella zoster virus (VZV), and rubella.
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
269 , hepatitis B (HBV), varicella zoster virus (VZV), measles, and mumps.
270  we examined whether varicella-zoster virus (VZV)-infected cells produce amyloid.
271 , we determined that varicella-zoster virus (VZV)-specific peak T helper 1 (VZV-Th1) responses to ZVL
272 fter reactivation of varicella zoster virus (VZV).
273 ex viruses (HSV) and varicella zoster virus (VZV).
274 with reactivation of varicella-zoster virus (VZV).
275 is B virus (HBV) and varicella-zoster virus (VZV).
276  work has shown that varicella-zoster virus (VZV; also called human herpesvirus 3 [HHV3]), the human
277 yet been reported in varicella-zoster virus (VZV; also known as human herpesvirus 3 [HHV-3]).
278 ic stimulation (with varicella-zoster virus [VZV] and cytomegalovirus [CMV]).
279  JC virus [JCV], and varicella-zoster virus [VZV]).
280 umps, rubella, and varicella-zoster viruses (VZV; MMRV) is a common condition of employment for healt
281                 The expression of four vital VZV genes, ORF61 and the genes for glycoproteins gC, gE,
282      Blocking the PD1 pathway during ex vivo VZV restimulation increased the CD4(+) and CD8(+) prolif
283 echnologies to study the mechanisms by which VZV infects human neurons.
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
287                    In luciferase assays with VZV open reading frame 61 (ORF61) promoter reporter plas
288 made in lytic infections and associated with VZV latency.
289          No large late endosomes filled with VZV particles were observed in Pompe cells; only individ
290 n electron microscopy, neurons infected with VZV produced fewer defective or incomplete viral particl
291                       Primary infection with VZV causes chicken pox.
292                 We found that a patient with VZV CNS vasculopathy had antibody that neutralized inter
293      Our results indicate that patients with VZV encephalitis suffer from cognitive impairment long t
294                       Thirteen patients with VZV encephalitis, diagnosed by detection of VZV DNA in c
295 arkers in a follow-up study of patients with VZV encephalitis.
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
299                                  At 3 years, VZV-CMI differences between groups decreased and only me
300  yellow-fever or varicella-zoster virus (YFV/VZV) vaccines was more suspended, with early IFN-associa

 
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