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1 s provide protection from symptomatic ocular herpes.
2 ated with protective immunity against ocular herpes.
3 sed immunotherapy to combat recurrent ocular herpes.
4 mmune checkpoints to combat recurrent ocular herpes.
5 ionship exists between tuberculosis risk and herpes coinfection.
6 established HLA Tg rabbit model of recurrent herpes highlight that blocking immune checkpoints combin
7  will help design future T-cell-based ocular herpes immunotherapeutic vaccines.IMPORTANCE A staggerin
8 t immune checkpoint targets to combat ocular herpes.IMPORTANCE HSV-specific tissue-resident memory CD
9 e immune response against symptomatic ocular herpes.IMPORTANCE We investigated the protective role of
10  a significant reduction in recurrent ocular herpes in HLA transgenic (Tg) rabbit model.
11 mportant strategy to combat recurrent ocular herpes in the clinic.
12 associated with protection against recurrent herpes infection and disease.
13 ated with protective immunity against ocular herpes infection and disease.IMPORTANCE We report that n
14 tiviral CD8(+) T cell exhaustion during SYMP herpes infection and pave the way to targeting immune ch
15 ucosa and provide protection against genital herpes infection in mice.
16 d, these cells protect hosts against genital herpes infection.
17 press replication or reactivation of chronic herpes infections.
18  viruses in the Herpesviridae family, causes herpes labialis (cold sores) and keratitis (inflammation
19                                      Typical herpes lesion site biopsy (TLSB) and cervical biopsy spe
20  severity and frequency of recurrent genital herpes lesions.
21                                              Herpes ocular infections was suspected.
22 in the guinea pig model of recurrent genital herpes, of subunit vaccine candidates that were based on
23 isms of protection against recurrent genital herpes remain to be fully elucidated.
24 ere highly prevalent in bile after LT, while herpes simpex virus 1 and 2 (HSV-1, HSV-2), varicella-zo
25                                        Fatal herpes simplex encephalitis (HSE) results from immune pa
26  infection (including cytomegalovirus [CMV], herpes simplex I/II or varicella zoster virus [HSV/VZV],
27                                       Ocular herpes simplex keratitis (HSK) is a consequence of viral
28                                              Herpes simplex keratitis (HSK), caused by herpes simplex
29 r clinical trial of 106 patients with active herpes simplex stromal keratitis who had not received an
30 flammation and in shortening the duration of herpes simplex stromal keratitis.
31 be structural organization of the virions of Herpes Simplex Type 1 viruses and bacteriophage MS2.
32 umanized monoclonal IgG antibody against the herpes simplex viral protein glycoprotein D (gD) was rad
33                               We developed a herpes simplex viral vector to rapidly yet transiently o
34 erpesviridae-positive, which included 9 with herpes simplex virus (8.8%), 5 with varicella-zoster vir
35 al fluid polymerase chain reaction (PCR) for herpes simplex virus (HSV) and varicella zoster virus wa
36                                              Herpes simplex virus (HSV) can cause severe infection in
37                                     Neonatal herpes simplex virus (HSV) disease results in unacceptab
38 the TG into the brain stem.IMPORTANCE Latent herpes simplex virus (HSV) DNA has been detected in the
39                                              Herpes simplex virus (HSV) establishes latency in neuron
40                                              Herpes simplex virus (HSV) establishes lifelong latent i
41                                              Herpes simplex virus (HSV) glycoprotein C (gC) functions
42                  We previously reported that herpes simplex virus (HSV) glycoprotein K (gK) binds to
43 of protein-protein interactions between four herpes simplex virus (HSV) glycoproteins (gD, gH/gL, and
44                                          The herpes simplex virus (HSV) heterodimer gE/gI and another
45 umcision was associated with reduced odds of herpes simplex virus (HSV) infection among MSM overall (
46     Numerous cases point to the link between herpes simplex virus (HSV) infection and multifocal CNS
47 ance frequently complicates the treatment of herpes simplex virus (HSV) infections in immunocompromis
48                                              Herpes simplex virus (HSV) is a common and often benign
49                                              Herpes simplex virus (HSV) is a neuroinvasive virus that
50                                              Herpes simplex virus (HSV) is among the most prevalent v
51 eity of cells expressing the LATs.IMPORTANCE Herpes simplex virus (HSV) is responsible for significan
52                                              Herpes simplex virus (HSV) is the main cause of viral en
53 d microparticles and a replication-defective herpes simplex virus (HSV) recombinant vector.
54                                              Herpes simplex virus (HSV) requires fusion between the v
55                                          The herpes simplex virus (HSV) single-strand DNA binding pro
56 s, systemic antimicrobial use, imaging data, herpes simplex virus (HSV) testing, and overall hospital
57 h as immunotherapy with oncolytic engineered herpes simplex virus (HSV) therapy, are urgently warrant
58 terial meningoencephalitis, 6% influenza, 6% herpes simplex virus (HSV), and 6% Mycoplasma pneumoniae
59       Anal swabs were collected to test HPV, herpes simplex virus (HSV), and 7 STIs.
60  to, HIV, respiratory syncytial virus (RSV), herpes simplex virus (HSV), and measles.
61 on of certain viruses, including poliovirus, herpes simplex virus (HSV), cytomegalovirus (CMV), and i
62  rather diverse glycan specificities such as Herpes Simplex Virus (HSV), Influenza A Virus (IAV), and
63 h diagnosed with-congenital cytomegalovirus, herpes simplex virus (HSV), varicella zoster virus (VZV)
64              The ubiquitous human pathogens, herpes simplex virus (HSV)-1 and HSV-2, are distinct vir
65                                              Herpes simplex virus (HSV)-1 proteins pUL7 and pUL51 for
66 ation in STING are unexpectedly resistant to Herpes Simplex Virus (HSV)-1, despite lacking STING-indu
67  TDRD7 is a viral restriction factor against herpes simplex virus (HSV-1).
68         One compound was also active against herpes simplex virus (HSV1 and HSV2), and another compou
69 ineered to constitutively express the type I Herpes Simplex Virus (HSV1) HSV-1 receptor, nectin-1, to
70 ockout (KO) mice were infected ocularly with herpes simplex virus 1 (HSV-1) (strain McKrae).
71                           In the case of the herpes simplex virus 1 (HSV-1) 0DeltaNLS vaccine, the co
72                                              Herpes simplex virus 1 (HSV-1) and HSV-2 can efficiently
73 ng assembly of the neurotropic herpesviruses herpes simplex virus 1 (HSV-1) and pseudorabies virus (P
74 strate that these cells can be infected with herpes simplex virus 1 (HSV-1) at a multiplicity of infe
75 rtive infections in HeLa cells infected with herpes simplex virus 1 (HSV-1) at high multiplicity of i
76 ILCs isolated from mice can be infected with herpes simplex virus 1 (HSV-1) but that subsequent repli
77                                              Herpes simplex virus 1 (HSV-1) can induce damage in brai
78                                              Herpes simplex virus 1 (HSV-1) can infect virtually all
79                                              Herpes simplex virus 1 (HSV-1) causes a lifelong infecti
80                                              Herpes simplex virus 1 (HSV-1) causes significant morbid
81                                              Herpes simplex virus 1 (HSV-1) cycles between phases of
82 rs such as bovine herpesvirus 1 (BoHV-1) and herpes simplex virus 1 (HSV-1) establish and maintain li
83 bility to reactivate from latency.IMPORTANCE Herpes simplex virus 1 (HSV-1) establishes a lifelong in
84                                              Herpes simplex virus 1 (HSV-1) establishes a lifelong la
85                   Following acute infection, herpes simplex virus 1 (HSV-1) establishes lifelong late
86                                              Herpes simplex virus 1 (HSV-1) establishes lifelong late
87 induced reactivation from latency.IMPORTANCE Herpes simplex virus 1 (HSV-1) establishes lifelong late
88                      Chronic viruses such as herpes simplex virus 1 (HSV-1) evade the hosts' immune s
89                An earlier report showed that herpes simplex virus 1 (HSV-1) expresses two microRNAs (
90              During all stages of infection, herpes simplex virus 1 (HSV-1) expresses viral microRNAs
91 is one of several cellular receptors used by herpes simplex virus 1 (HSV-1) for cell entry.
92                              Reactivation of herpes simplex virus 1 (HSV-1) from neurons in sensory g
93                  The Us11 protein encoded by herpes simplex virus 1 (HSV-1) functions to impair autop
94                                              Herpes simplex virus 1 (HSV-1) genes are transcribed by
95 i derived from the long-arm component of the herpes simplex virus 1 (HSV-1) genome, (iv) pUL36 serves
96                                              Herpes simplex virus 1 (HSV-1) has infected more than 80
97 e predicted 80 open reading frames (ORFs) of herpes simplex virus 1 (HSV-1) have been intensively stu
98 emethylation of histone H3K9 associated with herpes simplex virus 1 (HSV-1) immediate early (IE) prom
99                                          The herpes simplex virus 1 (HSV-1) immediate early protein I
100 the role of CD8(+) T cells in the control of herpes simplex virus 1 (HSV-1) infection and disease is
101 es have established a potential link between herpes simplex virus 1 (HSV-1) infection and the develop
102                                  Analysis of Herpes Simplex virus 1 (HSV-1) infection by population-a
103 onses following vaccination in resistance to herpes simplex virus 1 (HSV-1) infection continues to be
104                We have previously shown that herpes simplex virus 1 (HSV-1) infection results in the
105                    We recently reported that herpes simplex virus 1 (HSV-1) infection suppresses CD80
106 (-/-) mice were highly susceptible to ocular herpes simplex virus 1 (HSV-1) infection, independent of
107                                              Herpes simplex virus 1 (HSV-1) infects mucosal epithelia
108                                              Herpes simplex virus 1 (HSV-1) infects several types of
109          The envelope glycoprotein I (gI) of herpes simplex virus 1 (HSV-1) is a critical mediator of
110                                              Herpes simplex virus 1 (HSV-1) is a leading cause of inf
111 t of proteolipids in this process.IMPORTANCE Herpes simplex virus 1 (HSV-1) is a neurotropic pathogen
112 amatic displacement of the portal.IMPORTANCE Herpes simplex virus 1 (HSV-1) is the causative agent of
113                   Utilizing a mouse model of herpes simplex virus 1 (HSV-1) keratitis, we found that
114                 High rates of wild-type (WT) herpes simplex virus 1 (HSV-1) latency reactivation depe
115                       Corneal infection with herpes simplex virus 1 (HSV-1) leads to infection of tri
116 pectrometry approach, we have shown that the herpes simplex virus 1 (HSV-1) neurovirulence- and autop
117 le effect on cell-intrinsic immunity against herpes simplex virus 1 (HSV-1) or gammaherpesvirus 68 (g
118 ering number of the world population harbors herpes simplex virus 1 (HSV-1) potentially leading to bl
119 stimulates bovine herpesvirus 1 (BoHV-1) and herpes simplex virus 1 (HSV-1) reactivation.
120 terograde transneuronal tracers derived from herpes simplex virus 1 (HSV-1) strain 129 (H129) are imp
121                              The features of herpes simplex virus 1 (HSV-1) strain 129 (H129), includ
122                                      We used herpes simplex virus 1 (HSV-1) to infect the human DRG-d
123  stressful stimuli.IMPORTANCE The ability of herpes simplex virus 1 (HSV-1) to periodically reactivat
124 nd transmission to nerve endings, capsids of herpes simplex virus 1 (HSV-1) travel retrogradely withi
125                                              Herpes simplex virus 1 (HSV-1) triggers both the cyclic
126                           Here, we show that herpes simplex virus 1 (HSV-1) virions travel in associa
127 sidering the three groups, the prevalence of herpes simplex virus 1 (HSV-1) were 9% in saliva and 5%
128 e proportion of the world population harbors herpes simplex virus 1 (HSV-1), a major cause of infecti
129  protein 0 (ICP0), an E3 ubiquitin ligase of herpes simplex virus 1 (HSV-1), can derepress viral gene
130                                    Oncolytic herpes simplex virus 1 (HSV-1), devoid of the gamma(1)34
131                       In cells infected with herpes simplex virus 1 (HSV-1), hnRNPA2B1 was quantitati
132 al studies of the prototypical herpesviruses herpes simplex virus 1 (HSV-1), HSV-2, human cytomegalov
133 ocused on understanding the biology of human herpes simplex virus 1 (HSV-1), no tool has been develop
134 sosome-terminal endocytic pathway.IMPORTANCE Herpes simplex virus 1 (HSV-1), the prototype alphaherpe
135                                           In herpes simplex virus 1 (HSV-1)-infected cells, hnRNPA2B1
136  the more distantly related alphaherpesvirus herpes simplex virus 1 (HSV-1).
137 5beta, are activated early in infection with herpes simplex virus 1 (HSV-1).
138 GLF5 in Epstein-Barr virus (EBV), and vhs in herpes simplex virus 1 (HSV-1).
139 irus that can enter via the plasma membrane, herpes simplex virus 1 (HSV-1).
140 titer than other alphaherpesviruses, such as herpes simplex virus 1 (HSV1) or pseudorabies virus (PRV
141  that are derived from the DNA polymerase of herpes simplex virus 1 (Pol peptides).
142 aherpesviruses (pseudorabies virus [PRV] and herpes simplex virus 1 [HSV-1]).
143 EBV], human herpesvirus 6A [HHV-6A], HHV-6B, herpes simplex virus 1 [HSV-1], HSV-2, JC virus [JCV], a
144       This VZV study also complemented prior herpes simplex virus 1 and pseudorabies virus studies in
145  presence of brefeldin A, while studies with herpes simplex virus 1 documented an impaired secondary
146 -oligosaccharyltransferase with NGI-1 causes herpes simplex virus 1 dysfunction.
147 This disease can occur after reactivation of herpes simplex virus 1 in the trigeminal ganglia, leadin
148           Furthermore, time-lapse imaging of herpes simplex virus 1 infected epithelial cells enabled
149 owth within tumor cells.IMPORTANCE Oncolytic herpes simplex virus 1 is a promising agent for cancer i
150 polyfunctional antibody responses.IMPORTANCE Herpes simplex virus 1 is the leading cause of infectiou
151  selectively kill senescent cells expressing herpes simplex virus 1 thymidine kinase (HSV-TK).
152 virus, influenza virus, dengue virus type 2, herpes simplex virus 1, and nonenveloped human adenoviru
153  stomatitis virus, Semliki Forest virus, and herpes simplex virus 1, elicit the neuronal expression o
154  and higher incidence of cytomegalovirus and herpes simplex virus 1, possibly influenced by demograph
155  adults worldwide are latently infected with herpes simplex virus 1.
156     Human immunodeficiency virus (HIV-1) and herpes simplex virus 2 (HSV-2) affect hundreds of millio
157                              Reactivation of herpes simplex virus 2 (HSV-2) from latency causes viral
158  after the last virus inoculation.IMPORTANCE Herpes simplex virus 2 (HSV-2) infects nearly 500 millio
159                                              Herpes simplex virus 2 (HSV-2) is a common sexually tran
160 y(I.C) double-stranded RNA or infection with herpes simplex virus 2 (HSV-2).
161  in addition to one of three TAP inhibitors: herpes simplex virus 2 ICP47, bovine herpes virus 1 UL49
162 nced by certain microbial stimuli, including herpes simplex virus 2, and blocked by antibodies agains
163       Instead, upon secondary challenge with herpes simplex virus 2, circulating memory B cells that
164                  Thirteen patients (62%) had herpes simplex virus and 8 patients (38%) had varicella
165 revious reports linking TLR3 deficiency with herpes simplex virus encephalitis.
166                  Like all the herpesviruses, herpes simplex virus encodes machinery that enables it t
167 ly in stromal fibroblasts restores oncolytic herpes simplex virus function.
168 monly found bacterial pigment in controlling herpes simplex virus infection, for which diverse and mu
169                                       During Herpes Simplex Virus infection, viral replication compar
170 prevention of neonatal infections.IMPORTANCE Herpes simplex virus is among the most serious infection
171  activity during HSV-1 infections.IMPORTANCE Herpes simplex virus persists lifelong in neurons and ca
172 w that respiratory syncytial virus (RSV) and herpes simplex virus type 1 (HSV-1) accumulate a rich an
173              Here we report that GA inhibits Herpes simplex virus type 1 (HSV-1) by inhibition of bot
174           This study aimed at characterizing herpes simplex virus type 1 (HSV-1) epidemiology in the
175                                    Orolabial herpes simplex virus type 1 (HSV-1) infection has a wide
176    Herpes simplex keratitis (HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the co
177                                           In herpes simplex virus type 1 (HSV-1) infection, the coupl
178 ls associated with protective and pathogenic herpes simplex virus type 1 (HSV-1) infections remains u
179    Here we use direct RNA-seq to profile the herpes simplex virus type 1 (HSV-1) transcriptome during
180 asis of genome packaging and organization in herpes simplex virus type 1 (HSV-1), we developed sequen
181                                              Herpes simplex virus type 1 (HSV-1)-infected corneas can
182 t protective functions during infection with herpes simplex virus type 1 (HSV-1).
183 (mDCs) are not permissive for infection with herpes simplex virus type 1 (HSV-1).
184                                              Herpes simplex virus type 1 (HSV1) infection has been as
185 unravel the complexity of the interactome of herpes simplex virus type 1 (HSV1), the prototypical her
186                                          The herpes simplex virus type 1 thymidine kinase (HSV1-tk) g
187 une responses to chronic infections, such as herpes simplex virus type 2 (HSV-2) in HIV/HSV-coinfecte
188 f infection were seen in smokers, those with herpes simplex virus type 2 (HSV-2) infection, men who h
189 n to be at least tripled in individuals with herpes simplex virus type 2 (HSV-2) infection.
190                       Genital infection with herpes simplex virus type 2 (HSV-2) is common and increa
191                      This study investigated herpes simplex virus type 2 (HSV-2) seroprevalence utili
192           Interestingly, cells infected with herpes simplex virus type-1 (HSV-1) incorporated EdC and
193                                              Herpes simplex virus type-1 (HSV-1), one of the most wid
194 ed by the development of acyclovir-resistant herpes simplex virus viremia, primary graft failure, and
195 lium, Trichomonas vaginalis, adenovirus, and herpes simplex virus were absent.
196 ed virus, often an adeno-associated virus or herpes simplex virus, among many other types.
197 es were investigated for Epstein-Barr virus, herpes simplex virus, and HCMV-specific immunoglobulin G
198                                          For herpes simplex virus, this process requires the products
199 al response to HCMV, but not Epstein-Barr or herpes simplex virus, was associated with increased risk
200                                              Herpes simplex virus-1 (HSV-1) establishes a latent infe
201 gy is a powerful host defense that restricts herpes simplex virus-1 (HSV-1) pathogenesis in neurons.
202                                              Herpes simplex virus-1 (HSV-1) replicates within the nuc
203                 Neurotropic viruses, such as herpes simplex virus-1 (HSV-1), also rely on cellular AK
204              Infection by viruses, including herpes simplex virus-1 (HSV-1), and cellular stresses ca
205      Concordantly, GPX4 deficiency inhibited herpes simplex virus-1 (HSV-1)-induced innate antiviral
206 f several other pathogenic viruses including Herpes Simplex Virus-1 and-2, Vaccinia virus, and Zika v
207 ared to class B infections (cytomegalovirus, herpes simplex virus-1/2, human herpesvirus 8, hepatitis
208 e mechanisms underlying rapid elimination of herpes simplex virus-2 (HSV-2) in the human genital trac
209 ells.IMPORTANCE We study the pathogenesis of herpes simplex virus-mediated corneal disease.
210 -Barr virus (EBV), cytomegalovirus (CMV) and Herpes simplex virus.
211 that include the significant human pathogens herpes simplex viruses (HSV) and varicella zoster virus
212 ntain the same genetic variations.IMPORTANCE Herpes simplex viruses (HSV) infect a majority of adults
213 ults in Finland are seropositive carriers of herpes simplex viruses (HSV).
214  alphaherpesvirus related to human pathogens herpes simplex viruses 1 and 2 and varicella-zoster viru
215  transport of enveloped particles.IMPORTANCE Herpes simplex viruses 1 and 2 and varicella-zoster viru
216                                              Herpes simplex viruses bud into the nuclear membrane of
217 pesviruses such as varicella-zoster virus or herpes simplex viruses.
218 t human cells, DNA viruses such as vaccinia, herpes simplex, and adenovirus induced increased IFN pro
219 om patients with bacterial and viral (due to herpes simplex, varicella zoster, and enteroviruses) men
220  severity and frequency of recurrent genital herpes sores.
221                                              Herpes stromal keratitis (HSK) is a corneal chronic infl
222 blinding immunoinflammatory condition called herpes stromal keratitis (HSK), which involves the loss
223 n pathways play a fundamental role in ocular herpes T cell immunopathology and provide important immu
224 erging concept of developing an asymptomatic herpes vaccine that would boost effector memory CD4(+) a
225  the potential design of T-cell-based ocular herpes vaccines.
226 en AD or PD patients to those afflicted with herpes viral infections as to discover novel potential n
227  using anterograde transsynaptic conditional herpes viral tracing.
228 ch periodically replicate and produce viable herpes virions, particularly in anogenital and cervical
229 he latent phase, Kaposi's sarcoma-associated herpes virus (KSHV) maintains itself inside the host by
230  with infection by Kaposi sarcoma-associated herpes virus (KSHV).
231 RPP30) and a viral spike-in control (Phocine Herpes Virus 1 [PhHV-1]), which monitor sample quality a
232 bitors: herpes simplex virus 2 ICP47, bovine herpes virus 1 UL49.5, or rhesus cytomegalovirus Rh185.
233 irus (OR, 2.67; 95% CI, 1.75-4.36) and human herpes virus 6 (OR, 3.50; 95% CI, 1.15-10.63) were detec
234                The immune modulatory protein herpes virus entry mediator (HVEM) is one of several cel
235                  CD160 and BTLA both bind to herpes virus entry mediator.
236 of members of the enveloped filo, alpha, and herpes virus families but not the flavivirus group and n
237 cting these mice with EGFP-expressing murine herpes virus-68 (MHV68-EGFP) caused occasional transient
238   However, the patient had evidence of human herpes virus-6B infection.
239 is divided into idiopathic MCD (iMCD), human herpes virus-8 (HHV8)-associated MCD (HHV8-MCD), and pol
240 obes that cause persistent infections (e.g., herpes viruses) do so by switching from fast-growing lyt
241 eloped viruses, including influenza viruses, herpes viruses, and coronaviruses.
242 t defense against pathogenic viruses such as herpes viruses, flaviviruses, retroviruses, and coronavi
243  HSATII RNA in human cells infected with two herpes viruses.
244 of S. purpurea extracts against both pox and herpes viruses.
245 ly, using a rabbit model of recurrent ocular herpes, we found that the combined blockade of PD-1 and
246        The primary reported risk factors for herpes zoster (HZ) are increasing age and immunodeficien
247                             The incidence of herpes zoster (HZ) has been increasing in recent decades
248 dom (UK) due to concerns this could increase herpes zoster (HZ) incidence.
249        The primary reported risk factors for herpes zoster (HZ) include increasing age and immunodefi
250 compromised adults are at .increased risk of herpes zoster (HZ) infection and related complications.
251 ocompromised adults are at increased risk of herpes zoster (HZ) infection and related complications.
252              Efficacy of the live-attenuated herpes zoster (HZ) vaccine (ZVL) wanes substantially ove
253    The adjuvanted recombinant glycoprotein E herpes zoster (HZ) vaccine is superior to the live atten
254                  Data on the epidemiology of herpes zoster (HZ), particularly in the unvaccinated imm
255                  Data on the epidemiology of herpes zoster (HZ), particularly in the unvaccinated, im
256 and it can reactivate later in life, causing herpes zoster (HZ).
257       VZV causes varicella (chicken pox) and herpes zoster (shingles), while HCMV causes serious dise
258                  Information on the risks of herpes zoster (zoster) preceding a cancer diagnosis and
259 d indirect influences on the epidemiology of herpes zoster among children.
260 rld-wide, reactivating in one-third to cause herpes zoster and occasionally chronic pain.
261  category, and the annual rates of change in herpes zoster by age category, in an interrupted time se
262 oups revealed a net increase of hospitalized herpes zoster cases in individuals aged 10-49 years afte
263                                           No herpes zoster cases or major adverse cardiac events incl
264             Although the annual incidence of herpes zoster in adults has continued to increase, the r
265 has a substantial population-level impact on herpes zoster in nonvaccinated age groups.
266           Estimated vaccine efficacy against herpes zoster in patients with solid tumour malignancies
267 lysis on impact of chickenpox vaccination on herpes zoster incidence and time trend, focusing on popu
268                 The increase in age-adjusted herpes zoster incidence before implementation of chicken
269           In the antiretroviral therapy era, herpes zoster incidence continued to decline in people l
270                                              Herpes zoster incidence rates have continued to increase
271                                     Historic herpes zoster incidence trends in US adults have been ha
272 ccine effectiveness, duration of protection, herpes zoster incidence, and probability of postherpetic
273 tegories during 1996-2006 and 2007-2016, the herpes zoster incidences increased at annual rates of 1-
274                            In 1991-1995, the herpes zoster incidences increased at annual rates of 4-
275                     The annual incidences of herpes zoster increased throughout the period of 1991-20
276 sis showed a significant increase in risk of herpes zoster infection among patients who received JAK
277 meta-analysis, we found an increased risk of herpes zoster infection among patients with immune-media
278       Incidence rates of serious infections, herpes zoster infection, malignancy, and major cardiovas
279 mated incidence rates of serious infections, herpes zoster infection, non-melanoma skin cancer, other
280                                              Herpes zoster is linked to amyloid-associated diseases,
281 ion of chickenpox vaccination, incidences of herpes zoster may rise.
282 ied intention-to-treat population, confirmed herpes zoster occurred in 22 of 1328 (6.7 per 1000 perso
283 eatment of ophthalmoplegia in the setting of herpes zoster ophthalmicus (HZO) is controversial.
284                                              Herpes zoster ophthalmicus occurs primarily in elderly o
285                          We report a case of herpes zoster ophthalmicus-related ophthalmoplegia (HZOR
286      Outcome measures were the incidences of herpes zoster per 100 000 person-years, by calendar year
287                 The hypothesized increase in herpes zoster predicted from modelling of the exogenous
288 ng chemotherapy, but was not efficacious for herpes zoster prevention in patients with haematological
289 ccine was well tolerated and efficacious for herpes zoster prevention in patients with solid tumour m
290 ted varicella zoster virus (VZV) vaccine for herpes zoster prevention in patients with solid tumour o
291                       We evaluated pediatric herpes zoster trends using administrative databases.
292 thod to assess the safety of live attenuated herpes zoster vaccination during 2011-2017 in US adults
293 tinued to increase since introduction of the herpes zoster vaccines.
294 rated and estimated vaccine efficacy against herpes zoster was 16.8% (95% CI -17.8 to 41.3).
295                                              Herpes zoster was reported by one (<1%) patient on conti
296 PORTANCE Varicella-zoster virus (VZV) causes herpes zoster, a major health issue in the aging and imm
297 human alphaherpesvirus causing varicella and herpes zoster, expresses 24 virally encoded sncRNA (VZVs
298 cts a transient increase in the incidence of herpes zoster, peaking in adults 15-35 years after the s
299 ting wild-type varicella delays the onset of herpes zoster, predicts a transient increase in the inci
300  development of novel treatments for painful herpes zoster.
301 matological malignancies is at high risk for herpes zoster.

 
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