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1 prophylaxis against Pneumocystis carinii and varicella zoster.
2 and pneumonia, and an increase observed for varicella zoster.
4 varicella-zoster virus vaccine in preventing varicella-zoster and herpes zoster is well documented, a
5 smosis, other infections (such as syphillis, varicella-zoster, and parvovirus B19), cytomegalovirus,
6 reaction (PCR) analysis for Herpes simplex, varicella zoster, cytomegalovirus, Epstein-Barr virus an
7 ependent promoter and a model activator, the varicella zoster IE62 protein, it was determined that HC
9 number and critical immunization coverage of varicella-zoster infection in Belgium, Italy, Poland, an
11 virus (OPV), rubella, measles, yellow fever, varicella-zoster, multivalent measles/mumps/rubella, and
12 of herpes zoster disease, which is caused by Varicella zoster Nevertheless, the pathophysiological me
14 roidism, hypercholesterolemia, hypertension, varicella zoster, peripheral vascular disease, and autoi
15 clonal expansions in response to attenuated varicella-zoster vaccination in four pairs of adult iden
16 laria vaccine and the subunit glycoprotein E varicella zoster vaccine (both currently in phase III).
18 thy, such as prior herpes simplex keratitis, varicella-zoster viral keratitis, the linear form of Thy
21 s HSV1 and HSV2 (also termed HHV1 and HHV2), varicella zoster virus (VZV or HHV3), EBV (HHV4), cytome
22 tients showed a decreased ability to control varicella zoster virus (VZV) and Epstein-Barr virus (EBV
28 response biomarkers measuring antibodies to varicella zoster virus (VZV) by glycoprotein-based enzym
29 lex virus types 1 (HSV-1) and 2 (HSV-2), and varicella zoster virus (VZV) by weekly polymerase chain
30 se of herpes zoster caused by the attenuated varicella zoster virus (VZV) contained in Zostavax in a
31 , or no history of zoster (group 3) revealed varicella zoster virus (VZV) DNA in saliva samples from
32 rs who were immunized with Zostavax revealed varicella zoster virus (VZV) DNA in swabs of skin inocul
36 as an alternative to sampling of rashes for varicella zoster virus (VZV) genotyping and further char
37 s positive for herpes simplex virus (HSV) or varicella zoster virus (VZV) in 79% to 100% of cases of
38 Clinical reports observe the reactivation of varicella zoster virus (VZV) in people who have recovere
41 virus (CMV), herpes simplex virus (HSV), and varicella zoster virus (VZV) infections were monitored i
49 ne responses to a high-titer live attenuated varicella zoster virus (VZV) vaccine (zoster vaccine), w
50 Since the introduction of live attenuated varicella zoster virus (VZV) vaccine in 1995 there has b
52 portion of HZ cases caused by vaccine-strain varicella zoster virus (VZV), assessed the positive pred
53 c primers to detect DNA from JC virus (JCV), varicella zoster virus (VZV), cytomegalovirus (CMV), Eps
55 erpesviruses, herpes simplex virus (HSV) and varicella zoster virus (VZV), results in the rapid accum
56 immunogenicity of live-attenuated Oka/Merck varicella zoster virus (VZV)-containing vaccine (hereaft
58 We investigated the relationship between varicella zoster virus (VZV)-specific memory CD4(+) T ce
59 virus type 1 (HSV-1) and type 2 (HSV-2) and varicella zoster virus (VZV)-was determined in autonomic
63 RN, PCR-positive for herpes simplex virus or varicella zoster virus and evaluated between January 200
64 genes of both herpes simplex virus (HSV) and varicella zoster virus and functions, in part, by coupli
65 beyond CMV to other herpes viruses, such as varicella zoster virus and possibly Epstein-Barr virus.
66 ld decrease external boosting of immunity to varicella zoster virus and thereby increase incidence of
67 (as determined by testing lesions swabs for varicella zoster virus DNA by polymerase chain reaction)
68 ence of confirmed varicella (by detection of varicella zoster virus DNA or epidemiological link) from
71 were randomized 1:1 to receive either HZ/su (varicella zoster virus glycoprotein E; AS01B Adjuvant Sy
72 rveillance, combined with information from a Varicella Zoster Virus Identification Program, which use
73 cation) were associated with protection from varicella zoster virus infection (hazard ratio, 0.43; 95
74 contact dermatitis, infectious folliculitis, varicella zoster virus infection, fixed drug eruption, a
80 Because there is no good animal model of varicella zoster virus reactivation from latency, this e
81 -Barr virus, 3%; herpes simplex virus 1, 3%; varicella zoster virus, 3%; HHV7, 2%; and herpes simplex
82 ty of herpes simplex virus, cytomegalovirus, varicella zoster virus, and Epstein-Barr virus in our po
84 nstrate that childhood infections, including varicella zoster virus, are associated with an increased
85 for other infections (herpes simplex virus, varicella zoster virus, bacterial and fungal infections)
86 itis (AU), owing to either herpes simplex or varicella zoster virus, by using the Standardization of
87 se encephalitis virus, herpes simplex virus, varicella zoster virus, cytomegalovirus, dengue virus an
88 deficiency virus (HIV)-herpes simplex virus, varicella zoster virus, Epstein-Barr virus (EBV), and cy
89 gnificant members of the herpesvirus family: varicella zoster virus, human cytomegalovirus, and Epste
90 genes, Treponema pallidium, parvovirus, HIV, varicella zoster virus, Rubella, Cytomegalovirus, and He
91 highly dependent on the host cell, we tested varicella zoster virus-infected cell lysates and clinica
95 1), P. jirovecii pneumonia (1.77; .42-7.47), varicella-zoster virus (1.51; .71-3.22), as well as over
97 SV functioned as a monopartite NLS, while in varicella-zoster virus (VZV) activity required an adjace
98 are the main architectural contrasts between varicella-zoster virus (VZV) and herpes simplex virus (H
99 d the Us9 homologs from two human pathogens, varicella-zoster virus (VZV) and herpes simplex virus ty
102 simplex virus type 1 (HSV-1) is conserved in varicella-zoster virus (VZV) and pseudorabies virus (PRV
103 ype 1 (EHV-1), pseudorabies virus (PRV), and varicella-zoster virus (VZV) and their subsequent functi
105 gument proteins encoded by ORF11 and ORF9 of varicella-zoster virus (VZV) are conserved among all alp
107 Infection of human neurons in vitro with varicella-zoster virus (VZV) at a low multiplicity of in
110 Serum was tested for antibodies against varicella-zoster virus (VZV) by use of the previously va
113 highly infectious, human-restricted pathogen varicella-zoster virus (VZV) causes chickenpox and shing
114 ating VZV from clinical specimens.IMPORTANCE Varicella-zoster virus (VZV) causes chickenpox and shing
119 y throughout the study and were analyzed for varicella-zoster virus (VZV) DNA by use of both qualitat
126 ts had similar magnitude memory responses to varicella-zoster virus (VZV) ex vivo restimulation measu
131 tive target for antiviral therapy.IMPORTANCE Varicella-zoster virus (VZV) has infected over 90% of pe
133 umoral and cell-mediated immune responses to varicella-zoster virus (VZV) have been evaluated after 1
134 (EBV) EB2, herpes simplex virus (HSV) ICP27, varicella-zoster virus (VZV) IE4/ORF4, and cytomegalovir
137 ction by enveloped, but not cell-associated, varicella-zoster virus (VZV) in a dose-dependent manner
138 ects immediate-early protein IE63 encoded by varicella-zoster virus (VZV) in the cytoplasm of product
140 Previous studies have demonstrated that varicella-zoster virus (VZV) infection activates ERK1/2,
145 acaques (RMs) recapitulates the hallmarks of varicella-zoster virus (VZV) infection of humans, includ
147 he lytic, latent, and reactivating phases of varicella-zoster virus (VZV) infection were recapitulate
148 extensively studied the role of autophagy in varicella-zoster virus (VZV) infection, and have observe
157 The immediate early 62 protein (IE62) of varicella-zoster virus (VZV) is a major viral trans-acti
167 mary infection, latency, and reactivation by varicella-zoster virus (VZV) is incompletely understood.
177 f herpes simplex virus 1 (HSV-1), HSV-2, and varicella-zoster virus (VZV) on 695 consecutive cutaneou
188 f transcripts corresponding to all 68 unique varicella-zoster virus (VZV) open reading frames (ORFs)
192 In this report, we show that ORF61p, the varicella-zoster virus (VZV) ortholog of ICP0, does not
193 ced syncytium formation, a characteristic of varicella-zoster virus (VZV) pathology in skin and senso
194 this minireview is to provide an overview of varicella-zoster virus (VZV) phylogenetics and phylogeog
196 er acyclovir prophylaxis should be given for varicella-zoster virus (VZV) prophylaxis after hematopoi
199 nt is associated with increased incidence of varicella-zoster virus (VZV) reactivation in patients wi
200 IMPORTANCE The neurological damage caused by varicella-zoster virus (VZV) reactivation is commonly ma
201 a total of five major genotypes among the 22 varicella-zoster virus (VZV) strains or isolates for whi
205 r herpes simplex virus 1 (HSV-1), HSV-2, and varicella-zoster virus (VZV) to the BD Max system by usi
211 ish adverse events associated with wild-type varicella-zoster virus (VZV) versus those associated wit
214 The immediate early 62 protein (IE62) of varicella-zoster virus (VZV), a major viral trans-activa
217 1) and pseudorabies virus (PRV) and ORF66 in varicella-zoster virus (VZV), affects several viral and
220 pear healthy at 2 weeks after infection with varicella-zoster virus (VZV), and the cell culture mediu
221 ovirus, herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV).
222 sviruses, herpes simplex virus 1 (HSV-1) and varicella-zoster virus (VZV), confirmed the expression o
223 ults for herpes simplex virus 1/2 (HSV-1/2), varicella-zoster virus (VZV), cytomegalovirus (CMV), or
224 In this study, quantitative PCR detected varicella-zoster virus (VZV), herpes simplex virus 1 (HS
228 showed cytopathic changes, but HSV-1, unlike varicella-zoster virus (VZV), only rarely infected satel
230 cilitate the generation of mutant viruses of varicella-zoster virus (VZV), the agent causing varicell
231 nation was more likely to identify wild-type varicella-zoster virus (VZV), whereas the presence of Ok
233 the risk of herpes zoster (HZ), we compared varicella-zoster virus (VZV)-specific and nonspecific T-
235 n association with an age-related decline in varicella-zoster virus (VZV)-specific cell-mediated immu
236 udy were to evaluate the association between varicella-zoster virus (VZV)-specific humoral and cell-m
245 onal and pathogen-specific stimulation (with varicella-zoster virus [VZV] and cytomegalovirus [CMV]).
246 cropsy of two monkeys inoculated with simian varicella-zoster virus and euthanized 117 days later.
247 ia in adults includes common agents, such as varicella-zoster virus and influenza virus, as well as r
248 ate changes in the molecular epidemiology of varicella-zoster virus and the effect of immunization wi
251 e whether herpes zoster antigen (also called varicella-zoster virus antigen) was detectable in tempor
252 gical boosting, through which reexposures to varicella-zoster virus are thought to reduce the individ
256 the phenotypic spectrum of TLR3 mutations to varicella-zoster virus encephalitis and support the role
257 rpes zoster is a common late complication of varicella-zoster virus exposure and can be further compl
258 hus, a 30-h delay after death did not affect varicella-zoster virus expression in latently infected g
261 ve (at months 0, 1, 3) three doses of 50 mug varicella-zoster virus glycoprotein E (gE) adjuvanted wi
263 ubjects received 3 doses of HZ/su (50 microg varicella-zoster virus glycoprotein E [gE] combined with
264 g older adults, a subunit vaccine containing varicella-zoster virus glycoprotein E and the AS01B adju
265 zoster vaccine showed a greater increase in varicella-zoster virus gpELISA antibody compared with su
266 equences of wild-type and vaccine strains of varicella-zoster virus have been published and listed in
267 transfected cells, whereas expression of the varicella-zoster virus ICP22 homolog, ORF63, does not.
268 or who had resided in a country with endemic varicella-zoster virus infection for 30 years or more we
271 regulate infection of host cells.IMPORTANCE Varicella-zoster virus is an important human pathogen, w
275 -coinfected children and were independent of varicella-zoster virus or herpes-simplex virus 1 coinfec
276 lives ranging from an estimated 50 years for varicella-zoster virus to more than 200 years for other
277 ng heat-inactivated or replication-defective varicella-zoster virus to prevent HZ in immunocompromise
278 The continued success of the live attenuated varicella-zoster virus vaccine in preventing varicella-z
281 ty for CMV, EBV, herpes-simplex virus 1, and varicella-zoster virus were studied in 1079 6-year-old c
283 2, human herpesvirus 6, human parechovirus, varicella-zoster virus, and Cryptococcus neoformans/Cryp
284 antigens (vaccinia, measles, mumps, rubella, varicella-zoster virus, and Epstein-Barr virus) and nonr
285 Findings from skin biopsy, viral culture for varicella-zoster virus, and skin prick test to common fo
286 (HSV) and other alphaherpesviruses, such as varicella-zoster virus, depend upon the capacity to navi
287 es (parechovirus, dengue virus, Nipah virus, varicella-zoster virus, mumps virus, measles virus, lyss
288 h HLA-B27-associated (4460 [2465] pg/mL) and varicella-zoster virus-associated (5386 [1778] pg/mL) uv
290 in 50-59-year-old subjects were examined for varicella-zoster virus-specific antibody responses to va
291 1, CTLA-4, and TIM-3, whereas <2% of CMV- or varicella-zoster virus-specific CD4(+) T cells expressed
292 the change from baseline in IgG antibody to varicella-zoster virus-specific glycoproteins (gpELISA)
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