ライフサイエンスコーパス: VZV

1 VZV and human transcriptomes were concurrently investiga

2 VZV causes varicella (chickenpox), becomes latent in gan

3 VZV DNA was found in most aortas containing VZV antigen.

4 VZV establishes latency in the sensory ganglia and can r

5 VZV infection leads to increased autophagic flux, while

6 VZV is known to induce the formation of multinuclear cel

7 VZV mutants with both an ITIM mutation and either alanin

8 VZV syncytium formation, which has been implicated in th

9 informatics analyses identified more than 20 VZV-encoded 20- to 24-nucleotide RNAs, some of which are

10 Two of 4 VZV-inoculated RMs were challenged with SVV to determine

11 r virus (VZV) antibody titers (measured by a VZV glycoprotein-based enzyme-linked immunosorbent assay

12 ribute to their poor effector responses to a VZV challenge.

13 We used a VZV antigen challenge system in the skin to investigate

14 e, it was surprising to detect that VZV32, a VZV laboratory strain with no discernible growth defect

15 Overall, therefore, autophagy within a VZV-infected cell was remarkably different from autophag

16 the host-pathogen interactions during acute VZV infection in the lungs remain poorly understood due

17 at boost protective T cell responses against VZV.

18 An effective vaccine against VZV is available but not recommended for immunocompromis

19 on gamma inhibited not only the CPE but also VZV DNA accumulation, transcription, and virus productio

20 Although VZV infection is usually benign with few or no deleterio

21 Among VZV IgG-positive individuals, a higher percentage of VZV

22 emia with CMV, EBV, HHV-6, HSV-1, HSV-2, and VZV was detected in 60 (18%), 157 (48%), 80 (24%), 87 (2

23 ZV weekly reactivation probability at 5% and VZV subclinical reactivation having no effect on VZV-CMI

24 e evaluated human aortas for VZV antigen and VZV DNA.

25 in PD-L1 transcript levels between mock- and VZV-infected cells, indicating a posttranscriptional mec

26 nfected cells, full-length VZV proteins, and VZV peptides, as well as kill VZV-infected dermal fibrob

27 Here, we compare SVV and VZV with respect to interference with NF-kappaB activati

28 Given the homology between SVV and VZV, and the genetic and physiological similarities betw

29 ral clearance occurs in VZV vasculopathy and VZV infection of the lung is a step toward targeted ther

30 Using 3 different anti-VZV antibodies, we identified VZV antigen in 11 of 11 ao

31 PE) cell line, ARPE-19, with cell-associated VZV and compared its response to that of the MeWo cell l

32 esses leading to hyperfusion that attenuates VZV infection.

33 novel insight into the interactions between VZV and its human host and explain some of the neurologi

34 The relationship between VZV and its host during acute infection in the sensory g

35 hesis depended on known similarities between VZV gE and autophagy-related (Atg) Atg9/Atg16L1 traffick

36 Our in vitro system recapitulates both VZV latency and reactivation in vivo and may be used to

37 erminal kinase (JNK) pathway is activated by VZV infection and that blockade of this pathway limits l

38 sed for many years, the neuropathy caused by VZV infection is still a major health concern.

39 rame 47 (ORF47) and ORF66 kinases encoded by VZV.

40 ells, and probably the neuropathy induced by VZV infection.IMPORTANCE The neurological damage caused

41 et for intervention of neuropathy induced by VZV.

42 In rare cases, VZV can give rise to life-threatening disease in otherwi

43 referentially infecting skin-homing T cells, VZV alters cell signaling and remodels surface proteins

44 This may underlie their inability to contain VZV reactivation and prevent the development of HZ.

45 CA-negative participants whose TAs contained VZV antigen, 1 had histopathological features characteri

46 VZV DNA was found in most aortas containing VZV antigen.

47 ges in sections adjacent to those containing VZV were confirmed by 2 independent readers.

48 In contrast, VZV is highly infectious in vivo by airborne transmissio

49 bal gene activation at the site of cutaneous VZV antigen challenge compared with young subjects.

50 ion was associated with concurrent decreased VZV-memory and CD8(+) effector responses, respectively,

51 ; inhibition of autophagy leads to decreased VZV glycoprotein biosynthesis and diminished viral titer

52 gical relevance of these observations during VZV infection of human skin xenografts in the SCID mouse

53 g to pathological vascular remodeling during VZV vasculopathy and persistent inflammation in infected

54 mined memory CD4(+) T-cell responses to each VZV protein at baseline and after zoster vaccination.

55 Thus, effective VZV propagation is dependent on cell-cell fusion regulat

56 y an immunocompetent human host to eliminate VZV reactivation within neurons.

57 o the miRNA candidate significantly enhanced VZV plaque growth rates.

58 imized a targeted capture protocol to enrich VZV DNA and cDNA prior to whole-genome/transcriptome seq

59 high proportions of senescent and exhausted VZV-specific T cells in the older adults contribute to t

60 Despite formalin fixation, VZV DNA was detected in 2 of 4 GCA-positive, VZV antigen

61 f an otherwise healthy young male with focal VZV encephalitis, most likely acquired from VZV reactiva

62 respectively, we evaluated human aortas for VZV antigen and VZV DNA.

63 with cellular processes that are crucial for VZV pathogenesis.

64 ation and p300/CBP binding are important for VZV skin infection and may be targeted for antiviral dru

65 8H6 was characterized as a specific mAb for VZV ORF9, a membrane-associated tegument protein that in

66 dicating a posttranscriptional mechanism for VZV-mediated downregulation of PD-L1.

67 Notably, there is no animal model for VZV infection of the central nervous system.

68 gBcyt regulation is necessary for VZV pathogenesis, as the hyperfusogenic mutant gB[Y881F]

69 he viral genome copy number-to-PFU ratio for VZV in human neurons was 500, compared with 50,000 for M

70 is study, we found that ORF7 is required for VZV cytoplasmic envelopment in differentiated neuronal c

71 Neurons are major targets for VZV in vivo; in neurons, the virus can establish latency

72 y lead to better vaccines and treatments for VZV, since overcoming these mechanisms, either by small-

73 Cell-free VZV has been difficult to obtain, both for in vitro stud

74 VZV encephalitis, most likely acquired from VZV reactivation in the trigeminal ganglion.

75 oung adults had an increase in dual-function VZV-specific CD4(+) and CD8(+) T cell effectors defined

76 This process hinders VZV and is regulated by a viral glycoprotein, gB.

77 Historically, VZV is among the most genetically stable herpesviruses,

78 The findings further elucidate how VZV self-regulates multinuclear cell formation and may p

79 Overall, we define 13 novel CD4 and CD8 HSV-VZV cross-reactive epitopes and strongly imply additiona

80 ral proteins can harbor both CD4 and CD8 HSV/VZV cross-reactive epitopes.

81 Quantitative estimates of HSV/VZV cross-reactivity for both CD4 and CD8 T cells vary f

82 different anti-VZV antibodies, we identified VZV antigen in 11 of 11 aortas with pathologically verif

83 The induction of autophagy in VZV-infected monolayers is easily detectable; inhibition

84 ata suggest that reduced PD-L1 expression in VZV-infected adventitial cells contribute to persistent

85 bility complex class I (MHC-I) expression in VZV-infected cells and adjacent uninfected cells compare

86 s PD-L1 showed decreased PD-L1 expression in VZV-infected compared to mock-infected human brain vascu

87 An increase in VZV-stimulated CD4(+)CD69(+)CD57(+)PD1(+) and CD8(+)CD69

88 t, older adults showed marginal increases in VZV-specific CD8(+)CD57(+) senescent T cells after vacci

89 ial neurotropic gene, but its involvement in VZV replication is unclear.

90 MAPK, the c-Jun N-terminal kinase (JNK), in VZV lytic infection and reactivation.

91 rapies, identification of these molecules in VZV may provide a new direction for development of treat

92 ction with HSVDelta34.5, was not observed in VZV-infected cells.

93 sence of effective viral clearance occurs in VZV vasculopathy and VZV infection of the lung is a step

94 tification of the role of the JNK pathway in VZV infection of neurons reveals potential avenues for t

95 sm(s) by which inflammatory cells persist in VZV-infected arteries is unknown; however, virus-induced

96 autophagy, ICP34.5 and US11, not present in VZV.

97 tion sequencing (NGS) data for small RNAs in VZV-infected fibroblasts and human embryonic stem cell-d

98 es (MAPKs) have been shown to play a role in VZV infection of nonneuronal cells, with distinct conseq

99 gest that the SRT plays an important role in VZV viral gene expression and replication.

100 nce of VZV gene 9, 51, and 66 transcripts in VZV-infected human fetal lung fibroblasts was determined

101 The Oka/Merck varicella vaccine induces VZV immunity in elderly nursing home residents that is s

102 b11 proteins copurified with some infectious VZV particles.

103 Because intracerebral VZV vasculopathy and giant cell arteritis are strongly a

104 of erythema and induration after intradermal VZV antigen injection.

105 of virus with high titers, and for isolating VZV from clinical specimens.IMPORTANCE Varicella-zoster

106 proteins, and VZV peptides, as well as kill VZV-infected dermal fibroblasts.

107 causes chickenpox and reactivation of latent VZV causes herpes zoster (HZ).

108 s-react with VZV-infected cells, full-length VZV proteins, and VZV peptides, as well as kill VZV-infe

109 melanoma cells infected with wild-type-like VZV or hyperfusogenic mutants.

110 and survey cycle, odds ratios for a negative VZV IgG result in association with 1-unit increases in n

111 itical target for antibodies that neutralize VZV.

112 In contrast to the results for SVV DNA, no VZV DNA was detected in sensory ganglia at necropsy.

113 Cs, and HFLs, which, together with the noted VZV-mediated downregulation of MHC-I, might foster persi

114 The abundance of VZV gene 9, 51, and 66 transcripts in VZV-infected human

115 The low abundance of VZV nucleic acids in human neurons has hindered an under

116 Many aspects of VZV infection of sensory ganglia remain poorly understoo

117 ings indicate the need for authentication of VZV by sequencing when the virus is propagated in tissue

118 nserved between viruses from three clades of VZV.

119 ain some of the neurological consequences of VZV infection.

120 on upon VZV infection and reduced control of VZV replication.

121 correlates with the significant detection of VZV in granulomatous aortitis.

122 F7 deletion results in poor dissemination of VZV among neuronal cells.

123 Presence and distribution of VZV antigen in TAs and histopathological changes in sect

124 The cytoplasmic domain of VZV gB (gBcyt) has been implicated in cell-cell fusion r

125 )-based assay to determine the efficiency of VZV DNA shearing before ChIP, after which the assay was

126 clearly impacted cytoplasmic envelopment of VZV capsids, resulting in a dramatic increase of envelop

127 7 is required for cytoplasmic envelopment of VZV capsids, virus transmission among neuronal cells, an

128 CP34.5 ortholog, yet we found no evidence of VZV particles housed in a double-membraned autophagosome

129 VZV fusion protein, gB, in the formation of VZV induced multinuclear cells and in virus replication

130 arried out with highly purified fractions of VZV virions.

131 response characterized by the generation of VZV-specific antibodies and T cells.

132 a virus (SVV) recapitulates the hallmarks of VZV infection in humans.

133 es did not recapitulate all the hallmarks of VZV infection, including varicella, immunity, latency, a

134 h simian varicella virus (SVV), a homolog of VZV, provides a robust model of the human disease.

135 mechanisms underlying the immunopathology of VZV-associated posterior uveitis.

136 ith a peak threefold to fourfold increase of VZV-CMI; the VZV weekly reactivation probability at 5% a

137 Investigations of VZV-infected human brain from living immunocompetent hum

138 tein is a component of the tegument layer of VZV virions.

139 terminal domain of RNAP along the lengths of VZV genes (the promoter, body, and transcription termina

140 s production, thereby prolonging the life of VZV-infected neurons.

141 correlated negatively with the magnitude of VZV-specific responses.

142 te salivary VZV DNA as a surrogate marker of VZV reactivation and then to determine the utility of th

143 N-gamma) and interleukin 2 (IL-2; markers of VZV-specific cell-mediated immunity [CMI], measured by m

144 ge, we leveraged a nonhuman primate model of VZV infection where rhesus macaques are intrabronchially

145 d be facilitated by a robust animal model of VZV infection.

146 n skin xenografts in the SCID mouse model of VZV pathogenesis showed both that pCREB was upregulated

147 bined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that autophagosomes were

148 Open reading frame 7 (ORF7) of VZV has been recognized as a neurotropic gene in vivo, b

149 s of the virus parallels the pathogenesis of VZV in humans.

150 positive individuals, a higher percentage of VZV-specific T-cell-positive subjects was seen in those

151 xpected deletion of a significant portion of VZV ORF 12 following propagation in cultured human fibro

152 pected to reduce the pathogenic potential of VZV.

153 The presence of VZV antigen in granulomatous aortitis was highly signifi

154 with clinically suspected GCA, prevalence of VZV in their TAs is similar independent of whether biops

155 overall weighted seronegative prevalence of VZV was 2.2% for the pooled NHANES sample.

156 We show that the ORF61 proteins of VZV and SVV are sufficient to prevent IkappaBalpha ubiqu

157 Calculation of the incidence rate of VZV infection per 1000 patient-years was based on the re

158 Rates of VZV infections in clinical trials were low with fingolim

159 Rates of VZV infections in fingolimod clinical trials are based o

160 role in lytic infection and reactivation of VZV in physiologically relevant cell types and may provi

161 ted in a marked reduction in reactivation of VZV.

162 ith p300/CBP, restricted cell-cell spread of VZV in vitro CREB phosphorylation did not require the vi

163 tages compared to other cells for studies of VZV pathogenesis, for obtaining stocks of virus with hig

164 he results suggested that a subpopulation of VZV particles were carried to the cell surface in single

165 on the gene promoter, body, and terminus of VZV genes 9, 51, and 66.

166 he lung is a step toward targeted therapy of VZV-induced disease.

167 for their ability to produce high titers of VZV, the number of total virus particles relative to the

168 ed model that integrates within-host data on VZV-CMI and between-host transmission data to simulate H

169 investigated the effect of ORF7 deletion on VZV replication cycle at virus entry, genome replication

170 subclinical reactivation having no effect on VZV-CMI.

171 s hyperphosphorylated at serine 5 (S5(P)) on VZV genes 9, 51, and 66 independently of transcript abun

172 RC/94 epitope is in proximity to the site on VZV gHgL that activates gB.

173 , indicating that a residual effect of ZV on VZV-specific CMI persisted for >/= 10 years and was enha

174 At least one VZV sncRNA was expressed in productive infection of neur

175 hat memory PBMC expansion with either HSV or VZV enriches for CD4 T cell lines that recognize the oth

176 or IFN induction in response to synthetic or VZV-derived DNA.

177 dominant epitope located on gE, not on other VZV glycoproteins.

178 ic device with cell-free parental Oka (POka) VZV resulted in latent infection with inability to detec

179 VZV DNA was detected in 2 of 4 GCA-positive, VZV antigen-positive TAs.

180 Both baseline and postvaccination VZV-specific CMI were lower in the older age groups.

181 ted with higher baseline and postvaccination VZV-specific CMI.

182 ithstanding the mixture of variants present, VZV live vaccines are extremely stable.

183 nization for patients susceptible to primary VZV infection.

184 itis are strongly associated with productive VZV infection in cerebral and temporal arteries, respect

185 When purified VZV virions were enumerated after immunoelectron microsc

186 After recovery, VZV DNA and proteins were not detected in gastric biopsi

187 sed exaggerated syncytium formation, reduced VZV titers (-1.5 log10), and smaller plaques than with t

188 their functions are important for relieving VZV related neurological complications.

189 d this study demonstrates the first reported VZV-encoded sncRNAs.

190 hat of acyclovir, and an acyclovir-resistant VZV isolate was as sensitive to the effects of JNK inhib

191 We recommend establishing the patient's VZV immune status before initiating fingolimod therapy a

192 Detection of salivary VZV DNA in patients with abdominal pain helps to identif

193 hain reaction were used to validate salivary VZV DNA as a surrogate marker of VZV reactivation and th

194 of JNK inhibition as an acyclovir-sensitive VZV isolate in neurons.

195 We report 4 cases of acute severe VZV infection affecting the central nervous system or th

196 Antiviral drugs are effective against severe VZV infections but have little impact on PHN.

197 es confer increased susceptibility to severe VZV disease in otherwise healthy children, providing evi

198 Our results show VZV, like other human herpesviruses, encodes several snc

199 hesis was that ZVIN would elicit significant VZV-specific immune responses, measured by gpELISA or EL

200 ZVIN elicited a statistically significant VZV-specific immune response approximately 28 days post-

201 rated and elicited statistically significant VZV-specific immune responses approximately 28 days post

202 matic immunocompromised patients had similar VZV-specific immunologic properties except for lower T-c

203 hat human neurons may be useful for studying VZV in vitro, for growing preparations of virus with hig

204 e persons can be explained, in part, by such VZV cross-reactivity.

205 ere, we provide the first demonstration that VZV downregulates PD-L1 expression in infected HBVAFs, H

206 Although it is well established that VZV is transmitted via the respiratory route, the host-p

207 Our findings provide strong evidence that VZV transmission is seasonal and that seasonal peaks sho

208 access to human specimens and the fact that VZV is strictly a human virus.

209 Here, we report that VZV infection also induced CREB phosphorylation in fibro

210 de and seasonal timing, and (iv) reveal that VZV immunization significantly dampened seasonal cycles

211 We show that VZV grows to much higher titers in human neurons than in

212 The VZV genome lacks an ICP34.5 ortholog, yet we found no ev

213 ysis, points to the need to authenticate the VZV genome when the virus is propagated in tissue cultur

214 reefold to fourfold increase of VZV-CMI; the VZV weekly reactivation probability at 5% and VZV subcli

215 cluster (K894, K897, K898, and K900) in the VZV gBcyt was identified by sequence alignment to be con

216 powered to demonstrate noninferiority of the VZV antibody response at 6 weeks in the booster-dose gro

217 ine cluster in the cytoplasmic domain of the VZV fusion protein, gB, in the formation of VZV induced

218 analyses mapped to the repeat regions of the VZV genome, upstream of the predicted promoter of the im

219 The breadth and magnitude of the VZV-specific CD4(+) T-cell response increase after zoste

220 ic flux could exert a proviral effect on the VZV infectious cycle, we postulated that the VZV exocyto

221 Since the VZV genome is remarkably stable, it was surprising to de

222 VZV infectious cycle, we postulated that the VZV exocytosis pathway following secondary envelopment m

223 However, following vaccination, the VZV immune response increased in both cohorts, and no di

224 Therefore, VZV vaccination of RMs followed by SVV challenge is a mo

225 Thus, VZV may not necessarily have a higher particle-to-PFU ra

226 uses following incubation with antibodies to VZV gE ( approximately 100%), Rab11 (50%), and LC3B (30%

227 chicken pox information-seeking behavior to VZV vaccine-induced reduction of seasonal transmission.

228 These studies reveal mechanisms central to VZV pathogenesis, potentially leading to improved therap

229 to investigate a response by a human host to VZV infection.

230 Serological evaluation of immunity to VZV will help determine which individuals are susceptibl

231 throughput method for evaluating immunity to VZV.

232 Cross-reactivity to VZV is reconstituted by cloning and expressing TCRA/TCRB

233 Of note, the cellular response to VZV infection mimicked the response to other causes of t

234 In contrast, cutaneous responses to VZV antigen challenge were increased significantly in th

235 ut the cytokine and lymphocytic responses to VZV infection of RPE cells, thereby providing a useful p

236 ents displayed defective IFN production upon VZV infection and reduced control of VZV replication.

237 Varicella zoster virus (VZV) antibody titers (measured by a VZV glycoprotein-bas

238 eurons in vitro with varicella-zoster virus (VZV) at a low multiplicity of infection does not result

239 ) and 2 (HSV-2), and varicella zoster virus (VZV) by weekly polymerase chain reaction in plasma.

240 Varicella-zoster virus (VZV) causes chickenpox and reactivation of latent VZV ca

241 -restricted pathogen varicella-zoster virus (VZV) causes chickenpox and shingles.

242 specimens.IMPORTANCE Varicella-zoster virus (VZV) causes chickenpox and shingles.

243 Varicella-zoster virus (VZV) characteristically forms multinucleated cells, or s

244 rotropic herpesvirus varicella-zoster virus (VZV) establishes a lifelong latent infection in humans f

245 Varicella zoster virus (VZV) establishes latency in dorsal root, cranial nerve,

246 Varicella-zoster virus (VZV) establishes latency in human sensory and cranial ne

247 Varicella zoster virus (VZV) establishes lifelong persistence and may reactivate

248 memory responses to varicella-zoster virus (VZV) ex vivo restimulation measured by responder cell-fr

249 l therapy.IMPORTANCE Varicella-zoster virus (VZV) has infected over 90% of people worldwide.

250 euronal infection by varicella-zoster virus (VZV) have been challenging to study due to the relativel

251 mplex virus (HSV) or varicella zoster virus (VZV) in 79% to 100% of cases of suspected ARN.

252 the reactivation of varicella zoster virus (VZV) in people who have recovered from arsenic poisoning

253 role of autophagy in varicella-zoster virus (VZV) infection, and have observed that vesicular cells a

254 Varicella-zoster virus (VZV) infections increasingly are reported in patients wi

255 Varicella-zoster virus (VZV) is a common pathogen that causes chicken pox and sh

256 Varicella-zoster virus (VZV) is a highly contagious agent of varicella and herpe

257 62 protein (IE62) of varicella-zoster virus (VZV) is a major viral trans-activator and is essential f

258 Varicella-zoster virus (VZV) is a ubiquitous pathogen that causes chickenpox and

259 Varicella-zoster virus (VZV) is an alphaherpesvirus that causes varicella upon p

260 Varicella-zoster virus (VZV) is an extremely cell-associated herpesvirus with li

261 Varicella-zoster virus (VZV) is highly cell associated when grown in culture and

262 Varicella Zoster Virus (VZV) is the causative agent of varicella and herpes zost

263 a characteristic of varicella-zoster virus (VZV) pathology in skin and sensory ganglia.

264 cal damage caused by varicella-zoster virus (VZV) reactivation is commonly manifested as clinical pro

265 Studies of varicella-zoster virus (VZV) tropism for T cells support their role in viral tra

266 Varicella zoster virus (VZV) typically causes chickenpox upon primary infection.

267 Although a varicella-zoster virus (VZV) vaccine has been used for many years, the neuropath

268 the live-attenuated varicella-zoster virus (VZV) vaccine.

269 Varicella-zoster virus (VZV) vasculopathy produces stroke, giant cell arteritis,

270 s, and intracerebral varicella zoster virus (VZV) vasculopathy.

271 62 protein (IE62) of varicella-zoster virus (VZV), a major viral trans-activator, initiates the virus

272 imary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, results in varicel

273 Varicella-zoster virus (VZV), of the family Alphaherpesvirinae, causes varicella

274 icken pox, caused by varicella zoster virus (VZV), over an 11-y period.

275 Like varicella-zoster virus (VZV), simian varicella virus (SVV) reactivates to produc

276 attenuated Oka/Merck varicella zoster virus (VZV)-containing vaccine (hereafter, "varicella vaccine")

277 To measure varicella-zoster virus (VZV)-specific immune responses using glycoprotein enzyme

278 s to reactivation of varicella zoster virus (VZV).

279 e-divergent pathogen varicella zoster virus (VZV).

280 is B virus (HBV) and varicella-zoster virus (VZV).

281 with reactivation of varicella-zoster virus (VZV).

282 yet been reported in varicella-zoster virus (VZV; also known as human herpesvirus 3 [HHV-3]).

283 ic stimulation (with varicella-zoster virus [VZV] and cytomegalovirus [CMV]).

284 The expression of four vital VZV genes, ORF61 and the genes for glycoproteins gC, gE,

285 Blocking the PD1 pathway during ex vivo VZV restimulation increased the CD4(+) and CD8(+) prolif

286 avax and immunogenicity confirmed by ex vivo VZV-specific T-cell and antibody assays.

287 infection of neurons with vaccine Oka (VOka) VZV resulted in a latent infection similar to infection

288 immunofluorescence analyses to test whether VZV infection of adventitial cells downregulates PD-L1 s

289 and provide insight into mechanisms by which VZV infection can cause lung injury in an immune compete

290 echnologies to study the mechanisms by which VZV infects human neurons.

291 001) as compared to control aortas, in which VZV antigen was never associated with pathology, indicat

292 is activated upon infection of T cells with VZV.

293 abeling, both proteins also colocalized with VZV gE in a proportion of cytoplasmic vesicles.

294 n electron microscopy, neurons infected with VZV produced fewer defective or incomplete viral particl

295 lasts and neurons productively infected with VZV using TaqMan quantitative PCR (qPCR).

296 Interference with VZV T cell tropism may offer novel strategies for drug a

297 n virus-infected arteries from patients with VZV vasculopathy, while downregulation of MHC-I prevents

298 1-reactive CD8 T cells also cross-react with VZV-infected cells, full-length VZV proteins, and VZV pe

299 are nearly 100 times more permissive for WT VZV infection than very-early-passage human embryonic lu

300 em cells (hESC) and cell-free wild-type (WT) VZV, we demonstrated that neurons are nearly 100 times m