ライフサイエンスコーパス: HSV

1 HSV DNA was detected on 12% of days (IQR: 2 to 25%) from

2 HSV expressing the epitope from the full latency-associa

3 HSV induces host organelle rearrangement and forms multi

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

5 HSV-1 enters epithelial cells via an endocytosis mechani

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

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

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

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

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

11 HSV-2 antibody was detected in serum.

12 HSV-2 is a strong predictor of HIV epidemic potential am

13 HSV-2 prevalence of 25-49% indicates potential for inter

14 HSV-2 surveillance could inform HIV preparedness in coun

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 erpesviruses herpes simplex virus 1 (HSV-1), HSV-2, human cytomegalovirus (HCMV) and Epstein-Barr vir

50 ection even when viral load exceeded 1 x 107 HSV DNA copies, and surges in granzyme B and IFN-gamma o

51 ctions, such as herpes simplex virus type 2 (HSV-2) in HIV/HSV-coinfected persons, may sustain HIV ti

52 dy investigated herpes simplex virus type 2 (HSV-2) seroprevalence utility as a predictor of HIV epid

53 cy virus (HIV-1) and herpes simplex virus 2 (HSV-2) affect hundreds of millions of people worldwide.

54 NA or infection with herpes simplex virus 2 (HSV-2).

55 rapid elimination of herpes simplex virus-2 (HSV-2) in the human genital tract despite low CD8+ and C

56 ) developed the composite outcome (61 CMV, 3 HSV/VZV, 19 BSI, 10 IFI, 8 deaths).

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

58 perties, we investigated how it might affect HSV infection.

59 hown to be both safe and efficacious against HSV-2 and HIV-1 infections in vivo.

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

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

62 es ADCC provided complete protection against HSV disease and prevented the establishment of latency.

63 mmunization could provide protection against HSV for both mother and baby.

64 h therapeutic and vaccine strategies against HSV.IMPORTANCE Key to developing a human HSV vaccine is

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

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

67 -2, completely protected mice from HSV-1 and HSV-2 skin or vaginal disease and prevented latency foll

68 pathogens, herpes simplex virus (HSV)-1 and HSV-2, are distinct viral species that diverged approxim

69 Herpes simplex virus 1 (HSV-1) and HSV-2 can efficiently establish lifelong, transcriptiona

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

71 h increased likelihood of HSV-2 in women and HSV-2 in male partners.

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

73 se concerns about the use of live-attenuated HSV-2 vaccines in high HSV-1 prevalence areas.

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

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

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

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

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

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

80 e-cell RNA sequencing demonstrates that both HSV and individual AAV serotypes are non-randomly distri

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

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

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

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

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

86 acological approaches to better characterize HSV entry by endocytosis.

87 We analyzed shedding episodes during chronic HSV-2 infection; viral clearance always predominated wit

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

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

90 In adult mice, a single-cycle HSV candidate vaccine deleted in glycoprotein-D (DeltagD

91 A single-cycle HSV-2 strain with the deletion of glycoprotein D, Deltag

92 al immunization with a replication-defective HSV vaccine candidate, dl5-29, leads to transfer of viru

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

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

95 ttern of electrophysiological changes during HSV infection of DRG neurons, which may have implication

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

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

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

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

100 The intracellular itinerary for HSV entry remains unclear.

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

102 disrupts host signaling pathways needed for HSV growth and survival.

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

104 We found HSV genital shedding rates were positively correlated wi

105 and TLSB specimens in a woman with frequent HSV DNA shedding, with mixing of minor variants between

106 by UL46 are targeted by CD4(+) T cells from HSV-seropositive asymptomatic individuals (who, despite

107 gene expression were similar in corneas from HSV-CD80-infected and parental virus-infected mice.

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

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

110 sults in the greatest decrease in ganglionic HSV loads.

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

112 s herpes simplex virus type 2 (HSV-2) in HIV/HSV-coinfected persons, may sustain HIV tissue reservoir

113 Subclinical HSV shedding in HIV/HSV-coinfected women during ART may sustain HIV tissue r

114 l secretions were self-collected by nine HIV/HSV-2-coinfected women during ART for 28 days to establi

115 How HSV-1 structural proteins interact with ESCRT components

116 Our studies help elucidate how HSV gE/gI and US9 promote the assembly of virus particle

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

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

119 nst HSV.IMPORTANCE Key to developing a human HSV vaccine is an understanding of the virion glycoprote

120 Increasing evidence implicates HSV type 1 (HSV1) in the pathogenesis of late-onset Alzh

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

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

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

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

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

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

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

128 hways and promotes accelerated cell death in HSV-infected cells.

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

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

131 for significantly higher CD80 expression in HSV-CD80-infected mice, levels of HSV-1 gene expression

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

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

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

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

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

137 hway, resulted in only a slight reduction in HSV infection.

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

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

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

141 (TGN) functions and retrograde transport in HSV entry.

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

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

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

145 opes, but not with cryptic epitopes, induced HSV-specific polyfunctional IFN-gamma-producing CD107(ab

146 ractions with commensal bacteria may inhibit HSV infection, underscoring the importance of studying t

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

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

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

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

151 ing herpes simplex virus 1 thymidine kinase (HSV-TK).

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

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

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

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

156 otentially curative approach to treat latent HSV infection.

157 nd the subsequent packaging of a unit-length HSV genome.

158 ety and efficacy in a murine model of lethal HSV-2 infection.

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

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

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

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

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

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

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

166 The transport of nascent HSV particles from neuron cell bodies into axons and alo

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

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

169 ccine or cure, in part due to the ability of HSV to escape the host immune response by various mechan

170 ed after controlling for the total amount of HSV-specific IgG in the transferred serum.

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

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

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

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

175 nfection, prevented against a lethal dose of HSV-2 infection in a murine model.

176 We evaluate gene editing of HSV in a well-established mouse model, using adeno-assoc

177 s9, mediate highly efficient gene editing of HSV, eliminating over 90% of latent virus from superior

178 vide new information on antiviral effects of HSV-bacterial metabolite interactions.IMPORTANCE In this

179 ay lead to even more complete elimination of HSV.

180 -1 entry and suggest that endocytic entry of HSV-1 is independent of the canonical lysosome-terminal

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

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

183 In C57BL/6 mice, half of HSV-specific CD8(+) T cells (gB-CD8s) recognize one domi

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

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

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

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

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

189 The levels of HSV elimination observed in these studies, if translated

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

191 was associated with increased likelihood of HSV-2 in women and HSV-2 in male partners.

192 unoprecipitation experiments with lysates of HSV-infected neurons showed that UL16 and three other te

193 tants provide insights into the mechanism of HSV genome packaging.

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

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

196 utilized a human neuronal cell line model of HSV latency and reactivation (LUHMES) to characterize th

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

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

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

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

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

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

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

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

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

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

207 helial cells, which complicates the study of HSV assembly.

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

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

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

211 tabolite produced by Serratia marcescens, on HSV infection.

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

213 ination after lethal challenge with HSV-1 or HSV-2.

214 variation, and identified a strong positive HSV-2/HIV association.

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

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

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

218 lly deficient for the cGAS antagonist pUL41 (HSV-1DeltaUL41N) resulted in a cGAS-dependent type I int

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

220 to humans, would likely significantly reduce HSV reactivation, shedding, and lesions.

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

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

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

224 pted utilizing all single channels from RGB, HSV, and CieLab color space and all nonrepeating random

225 hone variation reduction, outperforming RGB, HSV, and CieLab color spaces.

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

227 tion of ganglionic CD8s, we examined several HSV recombinants that have different viral promoters dri

228 Subclinical HSV shedding in HIV/HSV-coinfected women during ART may

229 ing ART for 28 days to establish subclinical HSV DNA shedding rates and detection of HIV RNA by real-

230 Frequent subclinical HSV DNA shedding was associated with increased HIV DNA t

231 in two women with less frequent subclinical HSV DNA shedding.

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

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

234 Finally, we show that HSV cVAC formation and/or maintenance depends on an inta

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

236 We suggest that HSV has taken advantage of the adaptable nature of J pro

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

238 ecies recombination events have affected the HSV-2 genome, with recombinants and nonrecombinants at e

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

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

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

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

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

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

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

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

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

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

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

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

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

252 uggests a novel role for gC in shielding the HSV entry glycoproteins.

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

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

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

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

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

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

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

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

261 3D cultures of NPCs are less susceptible to HSV-1 infection than 2D cultures.

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

263 Two HSV membrane proteins, gE/gI and US9, play an essential

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

265 sed on the unique portal vertex of wild-type HSV and packaging mutants provide insights into the mech

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

267 Aged, diseased, human saphenous vein (HSV) remnants obtained from patients undergoing coronary

268 We now show that this recombinant virus (HSV-CD80) expressed high levels of CD80 both in vitro in

269 ain reaction (PCR) for herpes simplex virus (HSV) and varicella zoster virus was done in 237 (69%) an

270 Herpes simplex virus (HSV) can cause severe infection in neonates leading to m

271 Neonatal herpes simplex virus (HSV) disease results in unacceptable morbidity and morta

272 The herpes simplex virus (HSV) heterodimer gE/gI and another membrane protein, US9

273 Herpes simplex virus (HSV) is a neuroinvasive virus that has been used as a mo

274 Herpes simplex virus (HSV) is the main cause of viral encephalitis in the West

275 ial use, imaging data, herpes simplex virus (HSV) testing, and overall hospital charges.

276 itous human pathogens, herpes simplex virus (HSV)-1 and HSV-2, are distinct viral species that diverg

277 Herpes simplex virus (HSV)-1 proteins pUL7 and pUL51 form a complex required f

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

279 rpes simplex I/II or varicella zoster virus [HSV/VZV], blood stream infection [BSI], invasive fungal

280 of T2-weighted high-signal-intensity volume (HSV) and T2-weighted VIP independently, and the average

281 er treatment, a decrease in both T2-weighted HSV and T2-weighted VIP was observed (P = .03).

282 In participants with CF, T2-weighted HSV or T2-weighted VIP were associated with forced expir

283 range, 9-40 years]; eight men), T2-weighted HSV was equal to 0% and 4.1% (range, 0.1%-17%), respecti

284 t reactivation from latency.IMPORTANCE While HSV antivirals reduce the severity and duration of clini

285 nstrate that penile taxa are associated with HSV-2 in female partners, and vaginal taxa are associate

286 rtners, and vaginal taxa are associated with HSV-2 in male partners.

287 aplasma and Aerococcus) were associated with HSV-2 in women.

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

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

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

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

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

293 Compared to populations of FSWs with HSV-2 prevalence < 25%, adjusted odds ratios (AORs) of H

294 HIV prevalence was negligible in FSWs with HSV-2 prevalence <= 20% suggesting a threshold effect.

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

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

297 ased from 2.8 (95% CI 1.2-6.3) in those with HSV-2 prevalence 25-49%, to 13.4 (95% CI 6.1-29.9) in th

298 49%, to 13.4 (95% CI 6.1-29.9) in those with HSV-2 prevalence 75-100%.

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

300 At least 4 small, ancient HSV-1 x HSV-2 interspecies recombination events have affected th