ライフサイエンスコーパス: HSV infection

1 nt a new therapeutic strategy for inhibiting HSV infection.

2 ased risk of HIV infection in the setting of HSV infection.

3 ty-four adults had confirmed primary genital HSV infection.

4 ts a promising new class of vaccines against HSV infection.

5 inducible protein-10 (IP-10, CXCL10) during HSV infection.

6 this Ag resulting in protective immunity to HSV infection.

7 nding are stimulated during the course of an HSV infection.

8 6) and human beta-defensin (hBD) 3 inhibited HSV infection.

9 ial component of the immune response against HSV infection.

10 nitiates the postattachment (entry) phase of HSV infection.

11 sociation of the gD receptor is required for HSV infection.

12 cle in which mice are susceptible to vaginal HSV infection.

13 tical in determining the outcome of neonatal HSV infection.

14 dy and subsequent neonatal susceptibility to HSV infection.

15 induction of humoral responses to peripheral HSV infection.

16 r, but it could indicate resistance to overt HSV infection.

17 occurs in the corneal stroma in response to HSV infection.

18 ression of VP5 is a requirement for a normal HSV infection.

19 d mucous membranes, is the primary target of HSV infection.

20 d DNA replication, even with the presence of HSV infection.

21 association of the occurrence of EM with an HSV infection.

22 giogenesis and the severity of lesions after HSV infection.

23 a role, albeit probably a different role, in HSV infection.

24 ctions during intermediate to late stages of HSV infection.

25 elopment of immune modulatory treatments for HSV infection.

26 of plasmid DNA encoding CCR7 ligands before HSV infection.

27 paralysis-free survival during primary acute HSV infection.

28 ellular gene expression so characteristic of HSV infection.

29 cts had no clinical or virologic evidence of HSV infection.

30 role for vhs in modulating host responses to HSV infection.

31 ve sites and replication compartments during HSV infection.

32 underestimate overall prevalence of genital HSV infection.

33 oorly as shown by ELISA, and failed to block HSV infection.

34 yclovir, were tested in a mouse eye model of HSV infection.

35 m that may contribute to the pathogenesis of HSV infection.

36 for clinical investigation and diagnosis of HSV infection.

37 s for clinical and serologic evidence of new HSV infection.

38 ration which is targeted by VP16 to regulate HSV infection.

39 SV) is important in the control of recurrent HSV infection.

40 ficant change in Th subset balance following HSV infection.

41 ntibodies are relatively ineffective against HSV infection.

42 cephalitis, including 17 with disease due to HSV infection.

43 r the inability of this form of gDt to block HSV infection.

44 fic CTL response and provide protection from HSV infection.

45 tial role of these CTL in protection against HSV infection.

46 omatic relief from outbreaks but do not cure HSV infection.

47 an unexpected enhanced inhibitory effect on HSV infection.

48 ents are, and tree shrews are susceptible to HSV infection.

49 e control of local manifestations of primary HSV infection.

50 2, to investigate telomerase activity during HSV infection.

51 o date, there is no licensed vaccine against HSV infection.

52 study, we investigate role of telomerase in HSV infection.

53 d thus has pleiotropic inhibitory effects on HSV infection.

54 a highly prevalent chronic disease caused by HSV infection.

55 effort to induce greater protection against HSV infection.

56 regulate transcription of type I IFNs during HSV infection.

57 to generate a more effective vaccine against HSV infection.

58 cantly lower levels of corneal miR-132 after HSV infection.

59 ifferent mechanisms during various phases of HSV infection.

60 er was not tested, and those not at risk for HSV infection.

61 teraction of gamma(1)34.5 with TBK1 dictates HSV infection.

62 tected in IL-17 receptor knockout mice after HSV infection.

63 nce of neurons and other cells in the CNS to HSV infection.

64 s, were major producers of IL-17 early after HSV infection.

65 estions in the context of a murine cutaneous HSV infection.

66 n of T cells increased their permissivity to HSV infection.

67 t was not a measurement of the prevalence of HSV infection.

68 cted viruses in studying the early events in HSV infection.

69 otein ICP0 is a multifunctional regulator of HSV infection.

70 timulation was shown in both influenza A and HSV infections.

71 ising drug candidate for treatment of ocular HSV infections.

72 this technology for laboratory diagnosis of HSV infections.

73 and sensitivity to Vhs cleavage during lytic HSV infections.

74 tosis may be factors in the immunobiology of HSV infections.

75 their role in the pathogenesis of HIV-1 and HSV infections.

76 of viral tropism and damage during visceral HSV infections.

77 munity have significant problems controlling HSV infections.

78 fective for the majority of clinical VZV and HSV infections.

79 nt of severe and particularly drug-resistant HSV infections.

80 omen were followed for 20 months for primary HSV infections.

81 nd disease in mouse and guinea pig models of HSV infections.

82 the innate reaction to herpes simplex virus (HSV) infection.

83 of immune responses to herpes simplex virus (HSV) infection.

84 modifies experimental herpes simplex virus (HSV) infection.

85 oped EM secondary to a herpes simplex viral (HSV) infection.

86 which is triggered by herpes simplex virus (HSV) infection.

87 eonates with perinatal herpes simplex virus (HSV) infection.

88 flammatory response to herpes simplex virus (HSV) infection.

89 a very early event in herpes simplex virus (HSV) infection.

90 owed to be at risk for herpes simplex virus (HSV) infection.

91 that are resistant to herpes simplex virus (HSV) infection.

92 nd plays a key role in herpes simplex virus (HSV) infection.

93 nd in animal models of herpes simplex virus (HSV) infection.

94 ciency virus (HIV) and herpes simplex virus (HSV) infections.

95 identify 3 subject cohorts: 1 with no prior HSV infections, 1 with HSV-2 antibodies but no recognize

96 ed this hypothesis for herpes simplex virus (HSV) infection, a common OI in HIV+ patients.

97 HSV infection activates NF-kappaB pathways through Toll-

98 ave addressed the question of whether latent HSV infection affects neuronal gene expression by using

99 ion that could be exploited to better manage HSV infection, aid in vaccine design, or allow targeted

100 Here we show that HSV infection also induces phosphorylation of an endopla

101 HSV infection also results in the reorganization of the

102 sed the severity of ocular lesions caused by HSV infection, although no effects on this immunoinflamm

103 ere are marked differences in the outcome of HSV infection among the different neuronal populations i

104 iral vaccine, CJ9-gD, for protection against HSV infection and disease.

105 in protection of mice against neuroinvasive HSV infection and do so largely by mechanisms other than

106 beled murine sensory ganglia for evidence of HSV infection and for the sensory neuron marker A5 or KH

107 teen subjects were identified with an active HSV infection and had pre-outbreak, acute-phase, and pos

108 lain the lack of nerve damage from recurrent HSV infection and may provide insight to understanding a

109 s with these pharmacological agents inhibits HSV infection and prevents focal adhesion kinase (FAK) p

110 g parameter governing both the initiation of HSV infection and reactivation of latent genomes.

111 een, develop dysfunctional CD8+ T cells upon HSV infection and readily succumb to herpes encephalitis

112 phorylation of both serines was induced upon HSV infection and required functional ICP4 and ICP27.

113 Animals previously primed by HSV infection and subsequently given IL-10 DNA via the n

114 cose metabolism changed during the course of HSV infection and that modulating glucose levels can inf

115 ew revelations about these guardians against HSV infection and the consequences of the alarms raised

116 represent an important neuronal response to HSV infection and the establishment of latency.

117 t reductions in the symptoms associated with HSV infection and the symptomatic and asymptomatic shedd

118 ns cells (LC) obtained from AD patients with HSV infections and EH and nonatopic controls.

119 protein plays a role in the pathogenesis of HSV infections and that changing the expression kinetics

120 al role in controlling herpes simplex virus (HSV) infection and reactivation.

121 Autopsy confirmed disseminated HSV infection, and lung tissue grew acyclovir-resistant

122 ust to variation in test cost, prevalence of HSV infection, and random variation to study assumptions

123 ulted from nonneurologic causes unrelated to HSV infection, and three animals were sacrificed for his

124 of herpes labialis; 1 subject had a primary HSV infection; and 1 subject without baseline serology i

125 mportant manifestations and complications of HSV infection are considered here in a neuroanatomic con

126 The effects of CXCR3 signaling in HSV infection are strongly dependent on mouse strain.

127 Genital HSV infections are common and largely unrecognized among

128 Oral antiviral drugs for HSV infections are safe and effective and can be used bo

129 precise mechanisms that lead to generalized HSV infections are unknown.

130 ions that occur during herpes simplex virus (HSV) infection are not fully understood.

131 ptomatic mucocutaneous herpes simplex virus (HSV) infection are unclear.

132 Herpes simplex virus (HSV) infections are endemic, but the clinical characteri

133 istinction from viral infections, especially HSV infection, are of the utmost importance.

134 variable domain bound to virions and blocked HSV infection as well as HveC(346t).

135 oss is associated with herpes simplex virus (HSV) infection as deduced from epidemiologic data.

136 lls, were 16- to 50-fold more susceptible to HSV infection at the apical surface than at the basolate

137 The donors had no known active HSV infection at the time of death.

138 r early in the productive phase of wild-type HSV infection, but rather during establishment of a quie

139 rugs are used to treat herpes simplex virus (HSV) infection, but they cannot stop viral shedding and

140 PRO 2000 gel significantly inhibited HIV and HSV infection by at least 1000-fold, compared with CVL s

141 Soluble forms of gD (gDt) block HSV infection by interacting with specific cellular rece

142 nscriptase inhibitor to prevent both HIV and HSV infections by multiple mechanisms.

143 may shed light on the incomplete control of HSV infections by the immune system and may allow more r

144 These studies demonstrate that latent HSV infection can alter neuronal gene expression and mig

145 imulation molecules expressed at the site of HSV infection can enhance vaccine efficacy even in a ful

146 otent antiviral therapy during early primary HSV infection can reduce the magnitude of the latent inf

147 This work thus shows that (i) quiescent HSV infections can be maintained in PC12 cells in vitro,

148 Herpes simplex virus (HSV) infections can lead to cold sores, blindness, and b

149 effect of splicing on gene expression during HSV infection, cells were transfected with plasmids harb

150 ed with a diagnosis of herpes simplex virus (HSV) infection changed between 1985 and 1995.

151 and weaknesses of each method for diagnosing HSV infection, cite performance characteristics, and rev

152 ion of VZV-specific T-helper cell responses, HSV infections, CMV disease, chronic graft-versus-host d

153 Productive HSV infection colocalized with these receptors in SCG bu

154 physicians for genital herpes simplex virus (HSV) infection continue to increase.

155 cific T-cell immunity, herpes simplex virus (HSV) infection, cytomegalovirus (CMV) disease, survival,

156 were recorded regarding clinical evidence of HSV infection, degree of immune suppression, length of i

157 harged from the hospital with a diagnosis of HSV infection did not change over this time period despi

158 our understanding of host responses against HSV infection, discuss past clinical vaccine trials, and

159 percent or more of susceptible women acquire HSV infection during pregnancy.

160 ew the dual branches of HVEM function during HSV infection: entry and immunomodulation.

161 tory of recurrent oral herpes simplex virus (HSV) infections following dental treatment and antiviral

162 t identifies and types herpes simplex virus (HSV) infections for use in routine clinical settings.

163 sole receptor capable of enabling spread of HSV infection from the vaginal epithelium to the PNS and

164 Late in HSV infection, gE/gI, other viral glycoproteins, and env

165 Compared with the isolated pattern of HSV infection generally located in the center of control

166 erall, and children and mothers with chronic HSV infection had lower shedding rates than children wit

167 Mortality from neonatal HSV infection has fallen but remains high.

168 of regulation of NF-kappaB activation during HSV infection, highlighting the important role that NF-k

169 prone to disseminated herpes simplex virus (HSV) infection (ie, atopic dermatitis with a history of

170 mory CTL response to provide protection from HSV infection, immunized mice were challenged with a let

171 inst routine serologic screening for genital HSV infection in asymptomatic adolescents and adults, in

172 benefits of serologic screening for genital HSV infection in asymptomatic adolescents and adults, in

173 ing and preventive interventions for genital HSV infection in asymptomatic adults and adolescents to

174 w clear differences in the outcome of ocular HSV infection in CXCR2-/- compared with control BALB/c m

175 opes are targeted by the humoral response to HSV infection in humans.

176 class I-restricted T cells to the control of HSV infection in mice remains unclear.

177 fferent mechanisms for regulating productive HSV infection in neurons.

178 owever, some cellular mechanisms involved in HSV infection in rodents are different from those in hum

179 at IFN-gamma significantly attenuates latent HSV infection in the mouse model of ocular infection but

180 HSV infection in these cultured cells shows the properti

181 The pathogenesis of HSV infection in these mice may serve as a model of the

182 acrophages, and neutrophils all responded to HSV infection in vitro by up-regulating the expression o

183 nterfering RNA (siRNA) knockdown of Asf1a on HSV infections in HeLa cells.

184 antly, BILS 179 BS was orally active against HSV infections in murine models of HSV-1 and HSV-2 disea

185 l is quite different from the mouse model of HSV infection, in that the virus exhibited only a mild a

186 Serious consequences of HSV infection include neonatal herpes and increased risk

187 In addition, HSV infection induces a novel 70-kDa cellular protein de

188 roscopy of fluorescent viruses, we show that HSV infection induces the polarized migration of skin ce

189 hat ocular neovascularization resulting from HSV infection involves a change in the balance between V

190 lude that HSV viremia during primary genital HSV infection is common, especially among women.

191 understanding of the evolutionary aspects of HSV infection is crucial to the design of effective ther

192 The primary host response to HSV infection is the synthesis of stress response mRNAs

193 Herpes simplex virus (HSV) infection is a classic example of latent viral infe

194 Importance: Genital herpes simplex virus (HSV) infection is a prevalent sexually transmitted infec

195 Herpes simplex virus (HSV) infection is common in persons coinfected with huma

196 Primary genital herpes simplex virus (HSV) infection is commonly associated with systemic symp

197 Herpes simplex virus (HSV) infection is one of the most common opportunistic i

198 Herpes simplex virus (HSV) infection is restricted to epithelial cells and neu

199 Neonatal herpes simplex virus (HSV) infection is uncommon, but mortality after dissemin

200 Herpes simplex virus (HSV) infection is widespread in the human population.

201 utine serodiagnosis of herpes simplex virus (HSV) infections is currently performed using recombinant

202 a role in the protection of mice from lethal HSV infection, it does not substantively influence HSV r

203 Findings: Based on the natural history of HSV infection, its epidemiology, and the available evide

204 ting BBB permeability; and, in patients with HSV infection, magnetic resonance imaging-based temporal

205 pheral and central nervous systems following HSV infection may be important for resistance to reinfec

206 tory interactions for the control of primary HSV infection may represent a more widespread paradigm f

207 During HSV infection, nectin-1 localization at adherens junctio

208 During herpes simplex virus (HSV) infection, nuclear domain 10 (ND10) components loca

209 HSV infection shortly before labor, neonatal HSV infection occurred in four infants, of whom one died

210 the time of labor, 10 (5%) had neonates with HSV infection (odds ratio [OR], 346; 95% confidence inte

211 HSV infection of adult humans occasionally results in li

212 ence as the heptad repeat alpha-helix blocks HSV infection of B5-expressing porcine cells and human H

213 HSV infection of both CD4(+) and CD8(+) T cells occurred

214 o HVEM, and soluble BTLA and LTalpha blocked HSV infection of HVEM-expressing cells.

215 Finally, HSV infection of IL-17R knockout mice as well as IL-17 n

216 study the molecular events that occur during HSV infection of neurons.

217 Here, HSV infection of Oct-1-deficient mouse embryonic fibrobl

218 specific cellular receptors is essential for HSV infection of susceptible cells.

219 HSV infection of Tg-SCID mice was lethal, and mice faile

220 the role of CD8(+) T cells in the control of HSV infection of the central nervous system and suggest

221 We demonstrate here that HSV infection of the cornea results in the upregulation

222 In this study, we show that, after HSV infection of the cornea, IL-17 is upregulated in a b

223 at Robo4 receptors are upregulated following HSV infection of the eye on the majority of the new bloo

224 oach for limiting the angiogenesis caused by HSV infection of the mouse eye.

225 that (i) either HVEM or nectin-1 can permit HSV infection of the vaginal epithelium in mice and (ii)

226 ng the factors that determine the outcome of HSV infections of neurons.

227 N pathway have an elevated susceptibility to HSV infections of the CNS.

228 case of herpesviruses, herpes simplex virus (HSV) infection of epithelial cells results in a lytic in

229 Herpes simplex virus (HSV) infection of many cultured cells, e.g., Vero cells,

230 t, we demonstrate that herpes simplex virus (HSV) infection of the cornea results in the upregulation

231 hologic consequence of herpes simplex virus (HSV) infection of the cornea.

232 occurs in response to herpes simplex virus (HSV) infection of the mouse eye, which may serve to regu

233 Herpes simplex virus (HSV) infections of humans are characterized by intermitt

234 Studies of herpes simplex virus (HSV) infections of humans are limited by the use of rode

235 Herpes simplex virus (HSV) infections of the central nervous system (CNS) are

236 We evaluated the effects of HSV infection on keratinocytes, the initial target of HS

237 effect of a concurrent herpes simplex virus (HSV) infection on human immunodeficiency virus type 1 (H

238 -L were transiently upregulated after ocular HSV infection, on antigen-specific T cells and antigen-p

239 responses correlated with protection against HSV infection or disease.

240 effects of gD expression on nectin-1 during HSV infection or in transfected cells.

241 iver therapeutic cargos for the treatment of HSV infections or of dysfunctions of sensory ganglia.

242 However, at earlier times after HSV infection, or when gE/gI is expressed using virus ve

243 ngly, the expression of GADD34 stimulated by HSV infection parallels the status of eIF-2alpha phospho

244 AS to inhibit primary isolates of HIV, block HSV infection postentry, and cross cell membranes suppor

245 Herpes simplex virus (HSV) infections provoke an inflammatory cytokine respons

246 e clinical spectrum of herpes simplex virus (HSV) infections, ranging from asymptomatic to frequently

247 Neonatal HSV infection rates can be reduced by preventing materna

248 Neonatal HSV infection rates per 100 000 live births were 54 (95%

249 ldehyde-3-phosphate dehydrogenase, wild-type HSV infection reduced beta-actin mRNA levels to between

250 ions of sulforaphane into mice during active HSV infection reduced neuroinflammation via a decrease i

251 The generally mild medical consequences of HSV infection reflect a functional equilibrium between h

252 opment of treatments to prevent and/or treat HSV infection rely upon understanding viral and host fac

253 HSV infections remain a global health problem associated

254 HSV infections represent an incurable source of morbidit

255 COX-2 stimulation by HSV infection represents a critical early event accessib

256 Herpes simplex virus (HSV) infection requires binding of the viral envelope gl

257 strategies to prevent herpes simplex virus (HSV) infection requires knowledge of cellular pathways h

258 Surprisingly, HSV infection resulted in enhanced Treg function with su

259 ens from mice taken at different times after HSV infection revealed an early infiltration of plasmacy

260 ants born to nine women who acquired genital HSV infection shortly before labor, neonatal HSV infecti

261 Observations from experimental HSV infections suggest that antibodies could act in part

262 scordant donors had more frequent and severe HSV infections than those with HSV type-concordant donor

263 Together, these results support a model for HSV infection that requires activation of IP3-responsive

264 tal herpes is the high proportion of genital HSV infections that are unrecognized by both patients an

265 ur results shed light on the pathogenesis of HSV infections that lead to generalized infection and ac

266 In the context of natural HSV infection, the coupling of viral entry to the activa

267 ent protein kinase (PKR) is activated during HSV infection, the gamma(1)34.5 protein inhibits the act

268 man recombinant antibody in animal models of HSV infection, the present results support the high ther

269 During productive herpes simplex virus (HSV) infection, the viral transactivator VP16 associates

270 During lytic herpes simplex virus (HSV) infections, the half-lives of host and viral mRNAs

271 During lytic herpes simplex virus (HSV) infections, the HSV virion host shutoff protein (UL

272 During lytic herpes simplex virus (HSV) infections, the virion host shutoff (Vhs) (UL41) en

273 gI accumulates in the TGN in early phases of HSV infection then moves to lateral surfaces, to cell ju

274 1 as part of any vaccination regimen against HSV infection to coax responses of macrophages toward an

275 were able to limit the extent of a cutaneous HSV infection to comparable levels.

276 unction through the proteasome very early in HSV infection to inhibit a cellular antiviral response i

277 58 rabbit eyes before herpes simplex virus (HSV) infection to evaluate its intraocular antiviral dur

278 From analyses of HSV infections under various conditions, we conclude tha

279 T cells during acute and secondary stages of HSV infection using intracellular gamma interferon produ

280 e the latter for the laboratory diagnosis of HSV infections using LightCycler PCR.

281 ) mice are significantly more susceptible to HSV infection via the corneal and intracranial routes.

282 hus, expression of nectin-1 is necessary for HSV infection via the intracranial route and for encepha

283 Acute ocular HSV infection was accompanied by an intense leukocytic i

284 5 treatment before or at the time of initial HSV infection was an effective means of reducing the sev

285 ate the role of neutrophils in pathogenesis, HSV infection was compared in BALB/c and mice of the sam

286 ecessary step in the disease process, ocular HSV infection was followed in Tg-RAG mice (OVA-TCR trans

287 nancies for which the time of acquisition of HSV infection was known, 30 percent of the infections oc

288 Because the prevalence of HSV infection was similar across the groups, the elevate

289 A premature newborn with neurocutaneous HSV infection was treated for 21 days with acyclovir.

290 ating viral infection, herpes simplex virus (HSV) infection was assessed in mice that had the CD28/CD

291 nd foscarnet-resistant herpes simplex virus (HSV) infection was noted after lymphocyte-depleted blood

292 Both receptor binding and blocking of HSV infection were also affected by these C-terminal tru

293 lts with a first clinical episode of genital HSV infection were assayed for HSV DNA by polymerase cha

294 T cell-mediated immune responses to HSV infection were suppressed with this effect persistin

295 ts suspected of having herpes simplex virus (HSV) infections were processed using two different extra

296 eins move to cell junctions at late times of HSV infection when the production of enveloped particles

297 portion of women with a diagnosis of genital HSV infection who gave birth to infants by vaginal deliv

298 was identified which inhibited both HIV and HSV infections with no cellular toxicity.

299 become susceptible to the lethal effects of HSV infection, with the virus spreading to the brain cau

300 clinical or virological evidence of mucosal HSV infection yet possessed consistently detectable HSV-