ライフサイエンスコーパス: HSV-1

1 HSV-1 DNA has been detected in AD amyloid plaques in hum

2 HSV-1 enters epithelial cells via an endocytosis mechani

3 HSV-1 entry was unaltered in both cells treated with sma

4 HSV-1 infection caused similar relocalization phenotypes

5 HSV-1 infection of two-dimensional (2D) neuronal culture

6 HSV-1 may spread from infected to uninfected cells by tw

7 HSV-1 that lacks gC was more sensitive to complement-ind

8 HSV-1, on the other hand, has evolved several mechanisms

9 in NPCs infected at an MOI as low as 0.001, HSV-1 can establish a latent state, suggesting that (i)

10 hat GA inhibits Herpes simplex virus type 1 (HSV-1) by inhibition of both fusion and viral protein sy

11 characterizing herpes simplex virus type 1 (HSV-1) epidemiology in the Middle East and North Africa

12 HSK), caused by herpes simplex virus type 1 (HSV-1) infection, is the commonest cause of infectious b

13 In herpes simplex virus type 1 (HSV-1) infection, the coupling of genome replication and

14 and pathogenic herpes simplex virus type 1 (HSV-1) infections remains unclear.

15 Herpes simplex virus type 1 (HSV-1)-infected corneas can develop a blinding immunoinf

16 orld's population harbors latent HSV type 1 (HSV-1).

17 infection with herpes simplex virus type 1 (HSV-1).

18 s infected with herpes simplex virus type-1 (HSV-1) incorporated EdC and EdU at similar levels during

19 Herpes simplex virus type-1 (HSV-1), one of the most widely spread human viruses in t

20 fected ocularly with herpes simplex virus 1 (HSV-1) (strain McKrae).

21 In the case of the herpes simplex virus 1 (HSV-1) 0DeltaNLS vaccine, the correlate of protection ha

22 Herpes simplex virus 1 (HSV-1) and HSV-2 can efficiently establish lifelong, tra

23 tropic herpesviruses herpes simplex virus 1 (HSV-1) and pseudorabies virus (PRV) in the infected cell

24 cells infected with herpes simplex virus 1 (HSV-1) at high multiplicity of infection (MOI).

25 Herpes simplex virus 1 (HSV-1) can induce damage in brain regions that include t

26 Herpes simplex virus 1 (HSV-1) can infect virtually all cell types in vitro An i

27 Herpes simplex virus 1 (HSV-1) causes a lifelong infection of neurons that inner

28 Herpes simplex virus 1 (HSV-1) causes significant morbidity and mortality in hum

29 virus 1 (BoHV-1) and herpes simplex virus 1 (HSV-1) establish and maintain lifelong latent infections

30 m latency.IMPORTANCE Herpes simplex virus 1 (HSV-1) establishes a lifelong infection in neuronal cell

31 Herpes simplex virus 1 (HSV-1) establishes a lifelong latent infection in periph

32 stages of infection, herpes simplex virus 1 (HSV-1) expresses viral microRNAs (miRNAs).

33 ar receptors used by herpes simplex virus 1 (HSV-1) for cell entry.

34 Reactivation of herpes simplex virus 1 (HSV-1) from neurons in sensory ganglia such as the trige

35 Herpes simplex virus 1 (HSV-1) genes are transcribed by cellular RNA polymerase

36 arm component of the herpes simplex virus 1 (HSV-1) genome, (iv) pUL36 serves no direct role in cleav

37 ing frames (ORFs) of herpes simplex virus 1 (HSV-1) have been intensively studied for decades.

38 H3K9 associated with herpes simplex virus 1 (HSV-1) immediate early (IE) promoters and is necessary f

39 The herpes simplex virus 1 (HSV-1) immediate early protein ICP22 plays several roles

40 ls in the control of herpes simplex virus 1 (HSV-1) infection and disease is gaining wider acceptance

41 tential link between herpes simplex virus 1 (HSV-1) infection and the development of AD.

42 ion in resistance to herpes simplex virus 1 (HSV-1) infection continues to be rigorously investigated

43 reviously shown that herpes simplex virus 1 (HSV-1) infection results in the drastic spatial reorgani

44 cently reported that herpes simplex virus 1 (HSV-1) infection suppresses CD80 but not CD86 expression

45 Herpes simplex virus 1 (HSV-1) infects several types of cells, including neurons

46 ycoprotein I (gI) of herpes simplex virus 1 (HSV-1) is a critical mediator of virus-induced cell-to-c

47 Herpes simplex virus 1 (HSV-1) is a leading cause of infectious blindness, highl

48 s process.IMPORTANCE Herpes simplex virus 1 (HSV-1) is a neurotropic pathogen that can infect many ty

49 he portal.IMPORTANCE Herpes simplex virus 1 (HSV-1) is the causative agent of several pathologies ran

50 es of wild-type (WT) herpes simplex virus 1 (HSV-1) latency reactivation depend on the anti-apoptotic

51 have shown that the herpes simplex virus 1 (HSV-1) neurovirulence- and autophagy-modulating protein

52 virus 1 (BoHV-1) and herpes simplex virus 1 (HSV-1) reactivation.

53 tracers derived from herpes simplex virus 1 (HSV-1) strain 129 (H129) are important tools for mapping

54 The features of herpes simplex virus 1 (HSV-1) strain 129 (H129), including natural neurotropism

55 We used herpes simplex virus 1 (HSV-1) to infect the human DRG-derived neuronal cell lin

56 Herpes simplex virus 1 (HSV-1) triggers both the cyclic GMP-AMP synthase (cGAS)-

57 Here, we show that herpes simplex virus 1 (HSV-1) virions travel in association with MAL-positive s

58 s, the prevalence of herpes simplex virus 1 (HSV-1) were 9% in saliva and 5% in GCF; Epstein-Barr vir

59 ubiquitin ligase of herpes simplex virus 1 (HSV-1), can derepress viral genes by degrading ND10 orga

60 cells infected with herpes simplex virus 1 (HSV-1), hnRNPA2B1 was quantitatively exported to the cyt

61 ypical herpesviruses herpes simplex virus 1 (HSV-1), HSV-2, human cytomegalovirus (HCMV) and Epstein-

62 c pathway.IMPORTANCE Herpes simplex virus 1 (HSV-1), the prototype alphaherpesvirus, is ubiquitous in

63 In herpes simplex virus 1 (HSV-1)-infected cells, hnRNPA2B1 was quantitatively tran

64 Herpes simplex virus-1 (HSV-1) establishes a latent infection in neurons and per

65 Herpes simplex virus-1 (HSV-1) replicates within the nucleus coopting the host's

66 y viruses, including herpes simplex virus-1 (HSV-1), and cellular stresses cause widespread disruptio

67 deficiency inhibited herpes simplex virus-1 (HSV-1)-induced innate antiviral immune responses and pro

68 We conclude that abortive HSV-1 infection is a common feature during infection of

69 naturally exerts antiviral activity against HSV-1 and HSV-2 infections.

70 Sting(S365A/S365A) mice protect against HSV-1 infection, despite lacking the STING-mediated IFN

71 Additionally, PG protected against HSV-1 infection and disease progression in a murine mode

72 G CTT initiates protective responses against HSV-1, independently of type I IFNs.

73 in vivo Previously, we showed that although HSV-1 replication was similar in wild-type (WT) control

74 At least 4 small, ancient HSV-1 x HSV-2 interspecies recombination events have aff

75 V-1 immediate early transcription unit 1 and HSV-1 ICP0 promoters.

76 ss-talk between antiviral CD8(+) T cells and HSV-1 appear to control latency/reactivation cycles.

77 ays a key role in the egress of exosomes and HSV-1 from infected cells.

78 study shows that in the near absence of anti-HSV-1 antibody, vaccinated mice are protected from subse

79 expression systems, we demonstrate the anti-HSV-1 activity of TDRD7 in multiple human and mouse cell

80 lthough this axis is important for antiviral HSV-1 resistance, it has a pro-cancer role by promoting

81 their relative contributions in attenuating HSV-1 replication were found to be different in mouse ve

82 tatistically significant association between HSV-1 and HCMV was found in hemodialysis patients and se

83 ur study elucidates a new connection between HSV-1 egress, heparanase, and matrix metallopeptidases;

84 r, this paper shows a new connection between HSV-1 release and syndecan-1 shedding, a phenomenon that

85 NCE Growing evidence supports a link between HSV-1 infection and Alzheimer's disease (AD).

86 s are part of the initial tug of war between HSV-1 and host, which determines the ultimate outcome of

87 lopment of sensory neurons, could be binding HSV-1 genome directly to suppress viral gene expression

88 t that RUNX1, expressed highly in DRG, binds HSV-1 genome, represses transcription of numerous viral

89 with sphingosine enhancing compounds blocks HSV-1 propagation, suggesting a therapeutic potential of

90 actor TDRD7 inhibits AMPK and thereby blocks HSV-1 replication independently of the autophagy pathway

91 Alzheimer's disease (AD) proposes that brain HSV-1 infection could be an initial source of amyloid be

92 RTANCE Recurring ocular infections caused by HSV-1 can cause corneal scarring and blindness.

93 latency, the loss of VGSC activity caused by HSV-1 infection could not be blocked by ACV treatment.

94 also reported that overexpression of CD80 by HSV-1 exacerbated corneal scarring in BALB/c mice.

95 in understanding the mechanisms employed by HSV-1 to downregulate the anti-viral type I interferon (

96 To address how expression by HSV-1 influences the formation and ganglionic retention

97 that (i) NPCs can be efficiently infected by HSV-1, but infection does not result in cell death of mo

98 ) and VP11/12(483-497) epitopes presented by HSV-1-infected HLA-DR-positive target cells were recogni

99 The overall regulation of VGSCs by HSV-1 during quiescent infection was proved by increased

100 , suggesting that (i) a variant of classical HSV-1 latency can be established during earlier stages o

101 We screened for sgRNAs that cleave HSV-1 DNA sequences efficiently in vitro and used these

102 There are at least 20 confirmed HSV-1 miRNAs, yet the roles of individual miRNAs in the

103 ailing view and suggests that STING controls HSV-1 infection through IFN-independent activities.

104 We demonstrate HSV-1 reactivation from latently infected mouse neurons

105 fy a key determinant of this activity during HSV-1 infections.IMPORTANCE Herpes simplex virus persist

106 tifying activated cells within the TG during HSV-1 infection.IMPORTANCE Without an effective means of

107 MMP-7 were also naturally upregulated during HSV-1 infection.

108 CE Without an effective means of eliminating HSV-1 from latently infected neurons, efforts to control

109 ins of syndecan-1, thereby further enhancing HSV-1 egress from infected cells.

110 t patterns of Abeta42 accumulation following HSV-1 infection of 2D compared to 3D neuronal cultures (

111 associated Bro1 proteins are dispensable for HSV-1 replication.

112 specific for the major antigenic epitope for HSV-1 glycoprotein B (gB(498-505), gB) in C57BL/6 mice u

113 otein kinase (AMPK), which was essential for HSV-1 replication.

114 ults also identify new molecular markers for HSV-1 infection and new targets for future interventions

115 glycoprotein D (gD) but is not necessary for HSV-1 replication in vitro or in vivo Previously, we sho

116 from infected cells is an important step for HSV-1 transmission and virus-associated pathologies.

117 Conventional treatment for HSV-1 infection includes pharmaceutical drugs, such as a

118 D, DeltagD-2, completely protected mice from HSV-1 and HSV-2 skin or vaginal disease and prevented la

119 s suggest that genomes entering neurons from HSV-1 infections with strain KOS(M) are more prone to ra

120 successful treatment of active lesions (e.g. HSV-1, HSV-2 and varicella-zoster virus (VZV)).

121 the diverse receptor-binding glycoproteins (HSV-1 glycoprotein D (gD), EBV glycoprotein 42 (gp42) an

122 se of live-attenuated HSV-2 vaccines in high HSV-1 prevalence areas.

123 How HSV-1 structural proteins interact with ESCRT components

124 However, HSV-1 recombinant virus expressing cpIAP did not restore

125 However, HSV-1, unlike members of many other families of envelope

126 press the type I Herpes Simplex Virus (HSV1) HSV-1 receptor, nectin-1, to allow for more efficient in

127 Post-mortem and in vivo studies implicate HSV-1 infection in the brain as a precipitating factor i

128 ng loss of EAP20, HD-PTP, or BROX.IMPORTANCE HSV-1 is a pathogen of the human nervous system that use

129 ntial mechanism of immune evasion.IMPORTANCE HSV-1 causes lifelong infection in the human population

130 ned mechanisms in HSV-1 infection.IMPORTANCE HSV-1 ICP0 is a multifunctional immediate early protein

131 targets for future interventions.IMPORTANCE HSV-1 is a common cause of recurrent viral infections in

132 ye disease in HSV-1-infected mice.IMPORTANCE HSV-1 ocular infections are the leading cause of corneal

133 hment of latency and reactivation.IMPORTANCE HSV-1 is a common cause of ocular infections worldwide a

134 compare patterns of Abeta42 accumulation in HSV-1 infected 2D (neuronal monolayers) and 3D neuronal

135 and neural stem cell cultures, as well as in HSV-1-infected 3D neuronal culture models.The current st

136 However, the exact role of CD80 in HSV-1 immune pathology is not clear.

137 Antibody depletion of CD8(+) T cells in HSV-1 0DeltaNLS-vaccinated mice rendered animals highly

138 cells, leading to exacerbated eye disease in HSV-1-infected mice.IMPORTANCE HSV-1 ocular infections a

139 P-tau expression was transiently elevated in HSV-1-infected neurons, as well as in the presence of an

140 ential involvement of several Rab GTPases in HSV-1 entry and suggest that endocytic entry of HSV-1 is

141 mechanisms in PML II recognition by ICP0 in HSV-1 infection.

142 an-1 has not been previously investigated in HSV-1 release.

143 es showed Abeta42-immunoreactivity mainly in HSV-1-infected cells and only rarely in uninfected cells

144 nition via multiple fine-tuned mechanisms in HSV-1 infection.IMPORTANCE HSV-1 ICP0 is a multifunction

145 ld but a significant (>10-fold) reduction in HSV-1 released through the apical surface into the extra

146 Abeta accumulation was reported in HSV-1-infected 2D neuronal cultures and neural stem cell

147 t a likely case of transmitted resistance in HSV-1 between the patient and his brother, who also has

148 l activity of ICP27 that plays a key role in HSV-1-induced host shutoff and identify CPSF as an impor

149 owledge by showing how one insulator site in HSV-1 modulates lytic gene transcription and heterochrom

150 LA-A*0201 transgenic mice; and 2) in vivo in HSV-1-infected SYMP HLA-A*0201 transgenic mice.

151 rm response to persistent threats, including HSV-1 infection.IMPORTANCE Growing evidence supports a l

152 induced viral gene expression and increased HSV-1 infection in vitro In sum, these data support a no

153 eurons to become hyperexcitable also induced HSV-1 reactivation.

154 We found that SP-2509 does not inhibit HSV-1 IE gene expression or transcription factor and RNA

155 inoline compound Golgicide A (GCA) inhibited HSV-1 entry via beta-galactosidase reporter assay and im

156 When CD8(+) T cell responses are inhibited, HSV-1 can reactivate, and these recurrent reactivation e

157 also present the first analysis of intrahost HSV-1 evolution in an immunocompromised patient.

158 eactivation can occur at low frequency; (iv) HSV-1 impairs the ability of NPCs to migrate in a dose-d

159 ivo Transcriptome analysis detected 75 known HSV-1 genes in the corneas of mice infected with HSV-CD8

160 rom candidate viral promoters of "true late" HSV-1 genes either delayed or reduced the priming effici

161 ionic CD8(+) T cells during acute and latent HSV-1 infection.

162 teins is attributable to acute and/or latent HSV-1 infection in mature hippocampal neurons, a region

163 a indicate that viral promoters shape latent HSV-1-specific CD8(+) T cell populations and should be a

164 iplicities of infection (MOIs); (ii) limited HSV-1 replication and gene expression can be detected in

165 Lytic HSV-1 infections impaired NPC migration, which represent

166 e, Akt signaling correlates with maintaining HSV-1 latency in certain neuronal models of latency.

167 on represents a potential strategy to manage HSV-1 infections.

168 Mechanistically, HSV-1 replication after viral entry depended on AMPK but

169 n wild-type (WT) control and HVEM(-/-) mice, HSV-1 does not establish latency or reactivate effective

170 d from the cornea comparing vaccinated mice, HSV-1 0DeltaNLS-vaccinated animals possessed significant

171 value of hiPSC-derived 3D cultures to model HSV-1-NPC interaction.IMPORTANCE This study employed hum

172 DeltaNLS vaccine is effective against ocular HSV-1 challenge, reducing ocular neovascularization and

173 can library scanning of the entire 718 aa of HSV-1 VP11/12 sequence; (ii) an in silico peptide-protei

174 Through computational analysis of HSV-1 and HSV-2 genomes, we observed that putative RUNX

175 ING signaling pathways to the attenuation of HSV-1 infection.

176 LR3 and STING pathways to the attenuation of HSV-1 replication in mouse and human cell lines.

177 tures correlated well with the capability of HSV-1 to induce cell fusion in the UL24syn background, s

178 ver, compared to the asymptomatic corneas of HSV-1-infected WT mice, the symptomatic corneas CD1d KO

179 c nature of lytic versus latency decision of HSV-1 in nonneuronal cells.

180 erent times postnatally with lethal doses of HSV-1 or HSV-2.

181 -1 entry and suggest that endocytic entry of HSV-1 is independent of the canonical lysosome-terminal

182 The gB in the native envelope of HSV-1 had reduced reactivity with antibodies in comparis

183 t was noted that during the establishment of HSV-1 latency, the loss of VGSC activity caused by HSV-1

184 nificant impact on the basolateral export of HSV-1 from infected to uninfected cells by direct cell-t

185 Of note, exogenous expression of HSV-1 thymidine kinase increased the incorporation effic

186 The susceptibility and fate of HSV-1-infected NPCs are largely unexplored.

187 her, this work discovered a novel feature of HSV-1 gI that may have important implications in underst

188 Data showing inhibition of HSV-1 and CMV replication, when GA is administered post-

189 m cells (hiPSCs) to model the interaction of HSV-1 with NPCs, which reside in the neurogenic niches o

190 culture models to examine the interaction of HSV-1 with NPCs.

191 able model to investigate the involvement of HSV-1 in the onset of AD pathology.

192 future vaccine design.IMPORTANCE Latency of HSV-1 in host neurons enables long-term persistence from

193 t eye disease is independent of the level of HSV-1 replication and that viral expression of CD80 has

194 ression in HSV-CD80-infected mice, levels of HSV-1 gene expression were similar in corneas from HSV-C

195 We describe a novel mechanism of HSV-1 immune evasion via ICP22-dependent downregulation

196 eparanase, a recently identified mediator of HSV-1 release, syndecan-1 has not been previously invest

197 nges that underly HSK using a mouse model of HSV-1 corneal infection.

198 Utilizing an in vitro model of HSV-1 infection, we found that overexpressed RUNX1 could

199 ile changes of VGSCs during the processes of HSV-1 latency establishment and reactivation using human

200 es to characterize the resistance profile of HSV-1 in the patient and conclude that genotypic testing

201 s shed light on the biological properties of HSV-1 gI and may have important implications in understa

202 lts in a severe reduction in reactivation of HSV-1 in the mouse and rabbit models.

203 ntial new role for LSD1 in the regulation of HSV-1 DNA replication and gene expression after the onse

204 in Asah1(-/-) mice results in replication of HSV-1 and Asah1(-/-) mice die soon after systemic or int

205 urea extracts can inhibit the replication of HSV-1 by two distinct mechanisms of action.

206 sly been shown to inhibit the replication of HSV-1.

207 lts suggest that NPC pools could be sites of HSV-1 reactivation in the central nervous system (CNS).

208 ipation of MAL in the cell-to-cell spread of HSV-1 may shed light on the involvement of proteolipids

209 cycle, which reduces cell-to cell spread of HSV-1.

210 Strains of HSV-1 have been noted to vary greatly in their virulence

211 Strains of HSV-1 vary greatly in their virulence and potential to r

212 ithelial cells, which are natural targets of HSV-1 infection.

213 t of DNA replication.IMPORTANCE Treatment of HSV-1-infected cells with SP-2509 blocked viral DNA repl

214 replication experiments, the final yields of HSV-1 were unchanged following loss of EAP20, HD-PTP, or

215 and its ligands (LIGHT, CD160, and BTLA) on HSV-1 infectivity.

216 Once HSV-1 particles reach MVBs, sphingosine-rich ILVs bind t

217 ANCE Infecting 90% of the global population, HSV-1 and HSV-2 represent some of the most prevalent vir

218 loads ILVs with sphingosine, which prevents HSV-1 capsids from penetrating into the cytosol.

219 A critical step during productive HSV-1 infection is the cleavage and packaging of replica

220 nate antiviral immune responses and promoted HSV-1 replication in vivo.

221 MPORTANCE We report that naturally protected HSV-1-seropositive asymptomatic individuals develop a hi

222 As to observe the first editing of quiescent HSV-1 DNA.

223 hich has previously been shown to reactivate HSV-1 in rat neuron cultures.

224 T cell populations, we developed recombinant HSV-1 with the native immunodominant gB epitope disrupte

225 e relevant in light of observations relating HSV-1 infection to postencephalitic cognitive dysfunctio

226 xpression is recognized by ganglion-resident HSV-1-specific CD8(+) T cells that maintain a protective

227 This event demonstrates that resistant HSV-1 is transmissible among immunocompromised persons.

228 erienced recurrent infections with resistant HSV-1.

229 T cells with the same HLA-A*0201-restricted HSV-1 epitope specificities expressed multiple genes and

230 ctivities that are important for restricting HSV-1 infection, tumor immune evasion and likely also ad

231 n of memory CD8(+) T cells, sharing the same HSV-1 epitope-specificities, from infected HLA-A*0201 po

232 Akin to prior studies, HSV-1-infected 2D cultures showed Abeta42 immunoreactivi

233 mical inhibition of AMPK activity suppressed HSV-1 replication in multiple human and mouse cells.

234 a42 mainly in non-infected cells surrounding HSV-1-infected cells.

235 Here, we demonstrate that HSV-1 infection of iDCs and mDCs induces autophagy, whic

236 However, given that HSV-1 can overcome innate immune responses to establish

237 Understanding the impact that HSV-1 has on mature neurons and the proteins most strong

238 Clinical studies have also reported that HSV-1 causes postherpetic neuralgia and chronic occipita

239 Importantly, we show that HSV-1 catalyzes the aggregation of the amyloid beta-pept

240 Here, we show that HSV-1 forms an organized assembly factory in neuronal ce

241 Together, the data suggest that HSV-1 gC protects the viral envelope glycoproteins essen

242 iption and heterochromatin deposition as the HSV-1 genome establishes latency.

243 In transfected cells, the HSV-1 gI was discovered to induce rod-shaped structures

244 We characterized the HSV-1 pUL7:pUL51 complex by solution scattering and chem

245 Collectively, the HSV-1 0DeltaNLS vaccine is effective against ocular HSV-

246 a42 immunoreactivity in cells expressing the HSV-1 antigen ICP4 (ICP4+).

247 ltrating gB-specific CD8(+) T cells from the HSV-1 0DeltaNLS-vaccinated group.

248 two immunodominant epitopes derived from the HSV-1 tegument protein VP11/12.

249 dy, we report that several epitopes from the HSV-1 virion tegument protein (VP11/12) encoded by UL46

250 viral spread and pathogenesis.IMPORTANCE The HSV-1 gI is required for viral cell-to-cell spread withi

251 ble incorporation of the viral genome in the HSV-1 capsid.

252 NX1 could bind putative binding sites in the HSV-1 genome, repress numerous viral genes spanning all

253 ction of HVEM plays an important role in the HSV-1 latency and reactivation cycle that is independent

254 e is persistent viral gene expression in the HSV-1 latently infected TG.

255 protein key to effective replication in the HSV-1 lytic cycle and reactivation in the latent cycle.

256 A major function of the HSV-1 latency-associated transcript (LAT) is to establis

257 ein kinase is crucial for the ability of the HSV-1 latency-associated transcript (LAT) to inhibit apo

258 de a detailed map of Pol II occupancy on the HSV-1 genome that clarifies features of the viral transc

259 effects of the LSD1 inhibitor SP-2509 on the HSV-1 life cycle.

260 uencing to map and to quantify Pol II on the HSV-1(F) genome with single-nucleotide resolution.

261 y transcription unit 1 (IEtu1) promoter, the HSV-1 infected cell protein 0 (ICP0) promoter, and the m

262 ro and in vivo This suppression required the HSV-1 ICP22 gene.

263 oduce in this study can be used to study the HSV-1 genome in great detail to better understand viral

264 Here, we demonstrate that the HSV-1 immediate early protein ICP27 induces DoTT by dire

265 lization antibody titer in comparison to the HSV-1 0DeltaNLS-vaccinated wild-type C57BL/6 counterpart

266 tions is a key question in understanding the HSV-1 life cycle and pathogenesis.

267 Therefore, HSV-1 therapeutic approaches should focus on preventing

268 Thus, HSV-1 co-opts an innate immune pathway resulting from IL

269 es reach MVBs, sphingosine-rich ILVs bind to HSV-1 particles, which restricts fusion with the limitin

270 HVEM binds to HSV-1 glycoprotein D (gD) but is not necessary for HSV-1

271 Host mechanisms that contribute to HSV-1 egress from infected cells are poorly understood.

272 ed IFN responses and compromised immunity to HSV-1.

273 By contrast, resistance to HSV-1 is abolished in mice lacking the STING CTT, sugges

274 bute to the host adaptive immune response to HSV-1 challenge following vaccination with an attenuated

275 unit, resulted in defective IFN responses to HSV-1.

276 A difference in susceptibility to HSV-1 infection between two-dimensional (2D) and three-d

277 3D cultures of NPCs are less susceptible to HSV-1 infection than 2D cultures.

278 on, infected mice were highly susceptible to HSV-1 infection, and survival was partially but not sign

279 PSC)-derived cortical neurons susceptible to HSV-1.

280 The stimuli that trigger HSV-1 reactivation have not been fully elucidated.

281 Importantly, IL-1beta triggered HSV-1 reactivation, which was dependent on DLK and neuro

282 to characterize the latent infection of two HSV-1 wild-type strains.

283 ted from subsequent challenge with wild-type HSV-1 as measured by survival.

284 Here we show that macrophages take up HSV-1 via endocytosis and transport the virions into mul

285 ted by heparanase, which is upregulated upon HSV-1 infection.

286 RACs) increased propagation of the DNA virus HSV-1 but not the RNA virus VSV.

287 riction factor against herpes simplex virus (HSV-1).

288 While HSV-1 can remain static in an immunocompetent individual

289 While HSV-1 strain 17syn (+) can be readily reactivated, strai

290 e previously found that LSD1 associates with HSV-1 replication forks and replicating viral DNA, sugge

291 Infection of the reconstituted cells with HSV-1 revealed that both the cGAS-STING and the TLR3 sig

292 In contrast, infection of human T cells with HSV-1 that is functionally deficient for the cGAS antago

293 mice were resistant to ocular challenge with HSV-1 compared to vehicle-vaccinated animals based on su

294 al dissemination after lethal challenge with HSV-1 or HSV-2.

295 observed in vaccinated mice challenged with HSV-1, cornea pathology was mixed with a reduction in ne

296 Furthermore, Abeta(42) colocalized with HSV-1 latency-associated transcript (LAT) expression.

297 hippocampal neuronal cultures infected with HSV-1, with or without antivirals, were assessed for Abe

298 ell populations that survived infection with HSV-1 at high MOI.

299 of mitochondria that follows infection with HSV-1 was notably absent following Delta68-87 infection.

300 sgenic mouse (gBT-I.1) model vaccinated with HSV-1 0DeltaNLS.

301 produced pathogenic levels of VEGF-A within HSV-1-infected corneas, and CD4(+) cell depletion promot