ライフサイエンスコーパス: HSV-1

1 HSV-1 contributed more cases than HSV-2 in the Americas,

2 HSV-1 establishes latency within sensory neurons of trig

3 HSV-1 induced illness affects greater than 85% of adults

4 HSV-1 infection, unlike other HHV infections, caused acu

5 HSV-1 infections of the cornea range in severity from mi

6 HSV-1 manifests in a variety of clinical presentations r

7 HSV-1 recognized all sulfated GAGs, but not the nonsulfa

8 HSV-1's replication machinery includes a trimeric helica

9 HSV-1-reactive CD8 T cells also cross-react with VZV-inf

10 ters of EBOV or herpes simplex virus type 1 (HSV-1) in detergents-treated cell culture medium contain

11 infection with herpes simplex virus type 1 (HSV-1) induces profound modification of the cell nucleus

12 in immunopathogenesis of ocular HSV type 1 (HSV-1) infection.

13 Herpes simplex virus type 1 (HSV-1) is a leading cause of neurotrophic keratitis char

14 HSV type 1 (HSV-1) is a prevalent human pathogen that infects >3.72

15 otein D (gD) of herpes simplex virus type 1 (HSV-1) is one of four glycoproteins essential for HSV en

16 om mothers with herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2) genital infection.

17 ke all viruses, herpes simplex virus type 1 (HSV-1) reproduction relies upon numerous host energy-int

18 ighly defective herpes simplex virus type 1 (HSV-1) vectors that were functionally devoid of all vira

19 engineering of herpes simplex virus type 1 (HSV-1), which has a large DNA genome, using synthetic ge

20 murine model of Herpes Simplex Virus Type-1 (HSV-1) infection.

21 rus 6 (HHV-6), herpes simplex virus types 1 (HSV-1) and 2 (HSV-2), and varicella zoster virus (VZV) b

22 pathways.IMPORTANCE Herpes simplex virus 1 (HSV-1) afflicts 80% of the population worldwide, causing

23 Herpes simplex virus 1 (HSV-1) and HSV-2 are large, double-stranded DNA viruses

24 alphaherpesviruses, herpes simplex virus 1 (HSV-1) and pseudorabies virus (PRV), have suggested that

25 cted mice.IMPORTANCE Herpes simplex virus 1 (HSV-1) causes cold sores and neonatal herpes and is a le

26 Herpes simplex virus 1 (HSV-1) encodes the multifunctional neurovirulence protei

27 and is required for herpes simplex virus 1 (HSV-1) entry (1-3).

28 he dissection of the herpes simplex virus 1 (HSV-1) entry mechanism is complicated by the presence of

29 s the removal of the herpes simplex virus 1 (HSV-1) entry receptor Nectin-1 from the surface of infec

30 Herpes simplex virus 1 (HSV-1) establishes latency within the sensory neurons of

31 Herpes simplex virus 1 (HSV-1) establishes lifelong infection in the neurons of

32 helper virus such as herpes simplex virus 1 (HSV-1) for productive replication.

33 es expression of the herpes simplex virus 1 (HSV-1) gamma2 late genes by still unknown mechanisms.

34 o a small portion of herpes simplex virus 1 (HSV-1) glycoprotein D (gD) so that the first 40 amino ac

35 The herpes simplex virus 1 (HSV-1) ICP0 protein is an E3 ubiquitin ligase that promo

36 Herpes simplex virus 1 (HSV-1) infection is widespread among humans.

37 arly protein ICP0 of herpes simplex virus 1 (HSV-1) interacts with CIN85, an adaptor protein that aug

38 rt here that UL37 of herpes simplex virus 1 (HSV-1) is a protein deamidase that targets RIG-I to bloc

39 Human herpes simplex virus 1 (HSV-1) is a widespread pathogen, with 80% of the populat

40 tegument protein of herpes simplex virus 1 (HSV-1) is conserved among all herpesviruses and plays ma

41 Herpes simplex virus 1 (HSV-1) is one of the eight herpesviruses that can infect

42 d capsids.IMPORTANCE Herpes simplex virus 1 (HSV-1) is the causative agent of several pathologies ran

43 Herpes simplex virus 1 (HSV-1) latency entails the repression of productive ("ly

44 et the mRNA encoding herpes simplex virus 1 (HSV-1) major transcription regulator ICP4, which is esse

45 Herpes simplex virus 1 (HSV-1) most commonly causes recrudescent labial ulcers;

46 the live-attenuated herpes simplex virus 1 (HSV-1) mutant lacking the nuclear localization signal (N

47 uirement of UL21 for herpes simplex virus 1 (HSV-1) replication.

48 re HD10.6 neurons by herpes simplex virus 1 (HSV-1) results in a delayed but productive infection.

49 cular infection with herpes simplex virus 1 (HSV-1) sets off an inflammatory reaction in the cornea w

50 is virus (EMCV), and herpes simplex virus 1 (HSV-1) show impaired production of antiviral cytokines a

51 proteins encoded by herpes simplex virus 1 (HSV-1) that modulate type I IFN signaling.

52 pic alphaherpesvirus herpes simplex virus 1 (HSV-1) to enter neurons via axonal termini.

53 Herpes simplex virus 1 (HSV-1) UL20 plays a crucial role in the envelopment of t

54 The herpes simplex virus 1 (HSV-1) UL37 protein functions in virion envelopment at t

55 the live-attenuated herpes simplex virus 1 (HSV-1) VC2 vaccine strain, which has been shown to be un

56 epithelial tissues, herpes simplex virus 1 (HSV-1) virions travel via axonal transport to sensory ga

57 autophagy induced by herpes simplex virus 1 (HSV-1), encephalomyocarditis virus (EMCV) and influenza

58 ruses, such as human herpes simplex virus 1 (HSV-1), HSV-2, and veterinarian pseudorabies virus (PRV)

59 owing infection with herpes simplex virus 1 (HSV-1), PIAS1 is recruited to nuclear sites associated w

60 gument proteins from herpes simplex virus 1 (HSV-1), pUL7 and pUL51, which have homologues in all oth

61 esviruses, including herpes simplex virus 1 (HSV-1), stimulate mTORC1, how HSV-1-infected cells respo

62 is virus (VEEV), and herpes simplex virus 1 (HSV-1), suggesting that LIMK inhibitors could be develop

63 For herpes simplex virus 1 (HSV-1), we and others have previously published data dem

64 Herpes simplex virus 1 (HSV-1), which causes a variety of diseases, can establis

65 Although most herpes simplex virus 1 (HSV-1)-infected individuals shed the virus in their body

66 uring infection with herpes simplex virus 1 (HSV-1).

67 its helper viruses, herpes simplex virus 1 (HSV-1).

68 ularly infected with herpes simplex virus 1 (HSV-1).

69 Herpes simplex virus-1 (HSV-1) causes life-long morbidities in humans.

70 Herpes Simplex Virus-1 (HSV-1) is a ubiquitous human pathogen, which enters prod

71 Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) infect and establish latency in periphe

72 Viremia with CMV, EBV, HHV-6, HSV-1, HSV-2, and VZV was detected in 60 (18%), 157 (48%

73 hat utilizes the disialoganglioside GD2 as a HSV-1 entry receptor.

74 nd corticosterone selectively modulate acute HSV-1 and HSV-2 infections in autonomic, but not sensory

75 DEXxDSy showed high effectiveness against HSV-1 and HSV-2 viruses, as found using a variety of tec

76 Here, the role of IL-36 in immunity against HSV-1 was examined using the flank skin infection mouse

77 gy, yet the ability of Ab to protect against HSV-1 is deemed limited due to the slow IgG diffusion ra

78 an essential correlate of protection against HSV-1 pathogenesis and ocular pathology, yet the ability

79 ly unrecognized functions protective against HSV-1 infection.

80 tween viral and cellular factors that allows HSV-1 to enter host cells and establish infection.

81 s of the complex in the presence of ICP8, an HSV-1 protein that functions as an annealase, a protein

82 iscrepancy begs the question of how AAV2 and HSV-1 can coexist in a cell population.

83 iviral cytokines and-in the case of EMCV and HSV-1-reduced survival.

84 erived cells for the activities of IFI16 and HSV-1 ICP0.

85 Common ocular pathogens, such as HSV-1, are increasingly recognized as major contributors

86 We show that a live-attenuated HSV-1 vaccine elicits humoral immune responses that are

87 Here, we demonstrate that a live-attenuated HSV-1 vaccine has great translational potential.

88 ne was constructed using the live-attenuated HSV-1 VC2 vaccine strain.

89 This is important because HSV-1 reproduction triggered by physiological stress is

90 Here we describe novel interactions between HSV-1 and the DNA sensor STING.

91 nt understanding of the relationship between HSV-1 and its relevant in vivo target cell.

92 us macrophages (SSMs) exposed to lymph-borne HSV-1 were permissive only when type I interferon (IFN-I

93 y explained by an initial >457 basepair (bp) HSV-1 x HSV-2 crossover followed by back-recombination t

94 the environmental conditions encountered by HSV-1 when entering its host through the skin and emphas

95 antiviral IFN-beta effector is exploited by HSV-1 to establish an efficient replication domain in th

96 eratinocytes, IL-36alpha mRNA was induced by HSV-1, while IL-1beta and TNFalpha increased all three I

97 nd autonomic neurons that become infected by HSV-1 and HSV-2 express stress hormone receptors and are

98 were susceptible to secondary infections by HSV-1.

99 d that circulating HSV-2 strains can contain HSV-1 DNA segments in three distinct genes.

100 nsor STING plays pivotal role in controlling HSV-1 infection both in cell culture and in mice.

101 cyclovir are highly effective in controlling HSV-1 or -2 infections in immunocompetent individuals, t

102 The ability of AAV to cotransduce HSV-1-infected neurons in both the mouse and the rabbit

103 The cutaneous HSV-1 infection of mice results in the development of a

104 ty of U2OS and Saos-2 cells to the DeltaICP0 HSV-1 is in part due to an impaired STING pathway.IMPORT

105 Therefore, the DeltaICP0 HSV-1 virus is defective for growth in most cells, excep

106 ction of IFN-alpha/beta in the cornea during HSV-1 infection.

107 eceptor Nectin-1 is also internalized during HSV-1 infection in a Cbl-dependent mechanism, and that i

108 further investigate the role of MORC3 during HSV-1 infection.

109 the synthesis of proteins from mRNAs during HSV-1 infections.

110 factor which plays an important role during HSV-1 and HCMV infection.

111 UL46 counteracts the actions of STING during HSV-1 infection.

112 ar to modulate the functions of STING during HSV-1 infection.

113 UL7-pUL51 complex is important for efficient HSV-1 assembly and plaque formation.

114 The first oncolytic virotherapy employing HSV-1 (oHSV-1) was approved recently by the FDA to treat

115 cell epitopes was predicted from the entire HSV-1 genome.

116 Epithelial HSV-1 commonly infected myeloid cells, and Cre-Lox virus

117 lls release significantly less extracellular HSV-1 by 24 h postinfection (hpi), suggesting a unique n

118 Use of fluorescent HSV-1 virions demonstrated a pattern of viral spread ex

119 e of 14 000 cases annually roughly (4000 for HSV-1; 10 000 for HSV-2).

120 and this UL20 palmitoylation is required for HSV-1 infectivity.

121 ination of receptors distinct from those for HSV-1 or HSV-2 suggests a possible mechanism of enhanced

122 rise to distinct time-controlled windows for HSV-1 replication.

123 -1 neutralizing antibodies protect mice from HSV-1 eye disease, indicating the critical role of HVEM

124 rbates acute disease symptoms resulting from HSV-1 and HSV-2 infections and is associated with the ap

125 of a conserved tegument protein, UL37, from HSV-1.

126 High rates of genital HSV-1 infection and moderate HSV-2 prevalence meant the

127 mplex virus 1 (HSV-1), stimulate mTORC1, how HSV-1-infected cells respond to energy availability, a p

128 subtypes of the herpes simplex virus (HSV), HSV-1 and HSV-2.

129 levels of the alternative gD receptor HVEM, HSV-1 requires nectin-1, not HVEM, to enter these cells.

130 We found that (i) HSV-1 tegument protein UL46 interacts with and colocaliz

131 In this study, we show that (i) HSV-1 UL20 binds to GODZ (also known as DHHC3), a Golgi

132 ation of the recently FDA-cleared illumigene HSV 1&2 loop-mediated isothermal amplification (LAMP) as

133 parental strain in terms of immunogenicity, HSV-1 0DeltaNLS does not induce significant tissue patho

134 have the potential to differentially impact HSV-1 and HSV-2 so as to produce divergent outcomes of i

135 though stress hormones are thought to impact HSV-1 and HSV-2 through immune system suppression, senso

136 ol in the HSV-1 replicative cycle.IMPORTANCE HSV-1 infections are associated with a wide range of cli

137 ation regulates HSV-1 infectivity.IMPORTANCE HSV-1 UL20 is a nonglycosylated essential envelope prote

138 duce significant tissue pathology.IMPORTANCE HSV-1 is a common human pathogen associated with a varie

139 act mainly by the effects on Treg.IMPORTANCE HSV-1 infection has been shown to initiate an inflammato

140 eversible inactivation of virions.IMPORTANCE HSV-1 is an important pathogen with a high seroprevalenc

141 Here, we demonstrate that mTORC1 activity in HSV-1-infected cells is largely insensitive to stress in

142 these genome-wide epitopes were compared in HSV-1-seropositive symptomatic individuals (with a histo

143 gene and epistatic interaction discovery in HSV-1.

144 ase, indicating the critical role of HVEM in HSV-1 ocular infection.

145 hat disrupt miR-H2 without affecting ICP0 in HSV-1.

146 different roles these substrates may play in HSV-1 infection.

147 define more precisely the function of PML in HSV-1 replication, we constructed a PML(-/-) human cell

148 Following UV-B-induced HSV-1 reactivation, a significant increase in both the n

149 The synthesis and release of infectious HSV-1 and cell-to-cell spread of infection were all impa

150 2 phase support AAV2 replication and inhibit HSV-1 replication.

151 -dependent AAV2 DNA replication and inhibits HSV-1 DNA replication.

152 Instead, HSV-1 spread via the dorsal root ganglia to the autonomi

153 analysis of trigeminal ganglia from latently HSV-1-infected, glutamine-treated WT mice showed upregul

154 g the rate of HSV-1 reactivation in latently HSV-1-infected IFN-gamma-KO mice.

155 amine reduced virus reactivation in latently HSV-1-infected mice and HSV-2-infected guinea pigs.

156 hat they are capable of cell entry and, like HSV-1, require all four entry glycoproteins along with a

157 zacytidine (Aza; a cytosine analog) to limit HSV-1-induced ocular lesions.

158 ells do not play a major role in maintaining HSV-1 latency and reactivation.

159 RAW264.7 macrophage and PM in vitro models, HSV-1 replication in M1 macrophages was markedly lower t

160 Moreover, HSV-1 was able to enter keratinocytes but not other cell

161 argets Sp100, also augments ICP0-null mutant HSV-1 replication.

162 timulate the replication of ICP0-null mutant HSV-1, while ICP0 increases plaque formation by pp71-def

163 otection against corneal neovascularization, HSV-1 shedding, and latency through passive immunization

164 ibodies were able to specifically neutralize HSV-1 infection in vitro via HVEM.

165 and showed that these antibodies neutralized HSV-1 infection in cells expressing HVEM, but not the ot

166 M binding domain of HSV-1 gD (i) neutralized HSV-1 infection in a cell receptor-specific manner, (ii)

167 gnized a broader selection of nonoverlapping HSV-1 epitopes, (ii) expressed higher levels of PD-1, TI

168 f MORC3 resulted in an increase in ICP0-null HSV-1 and wt HCMV replication and plaque formation; ther

169 the cornea impeded protection against ocular HSV-1 challenge in vaccinated mice.

170 s opposed to subunit vaccines against ocular HSV-1 infection.

171 ther improve vaccine efficacy against ocular HSV-1 replication and latency.

172 ctivated or polarized) macrophages in ocular HSV-1 infection.

173 A very intriguing aspect of HSV-1 corneal infection is that the virus spread is norm

174 Blocks of >244 and >539 bp of HSV-1 DNA within genes UL29 and UL30, respectively, have

175 es the importance of STING in the control of HSV-1.

176 insights into the cholesterol dependence of HSV-1 replication.

177 nd 95.5%, respectively, for the detection of HSV-1.

178 OH) for the detection and differentiation of HSV-1 and HSV-2 in cutaneous and mucocutaneous swab spec

179 e and atypical lymphotropic dissemination of HSV-1 following ocular infection.

180 s vaccinated with the HVEM binding domain of HSV-1 gD (i) neutralized HSV-1 infection in a cell recep

181 ne that contained the HVEM binding domain of HSV-1 gD fused to HIV gp120.

182 cted HCE cells at three different dosages of HSV-1 and measured the outcomes in terms of viral entry,

183 ole for cellular cholesterol in the entry of HSV-1 into target cells.

184 asked whether a single transient episode of HSV-1 epithelial keratitis causes long-term changes in t

185 ns that are integral to the establishment of HSV-1 latency, to the maintenance of latency, and to rea

186 We applied previous estimates of HSV-1 and HSV-2 prevalence and incidence in women aged 1

187 mma134.5 gene product, a virulence factor of HSV-1, facilitates nuclear egress cooperatively with cel

188 at the four essential entry glycoproteins of HSV-1 are not only required but also sufficient for cell

189 signaling on virulence and immunogenicity of HSV-1 0DeltaNLS and uncover a probable sex bias in the i

190 also gives rise to a specific inhibition of HSV-1 late gene expression.

191 atment significantly increased the levels of HSV-1 DNA replication and production of viral progeny in

192 M2 macrophages directly reduce the levels of HSV-1 latency and, thus, T-cell exhaustion in the TG of

193 Levels of HSV-1 specific antibodies, CD8(+) cells and IFNgamma-pro

194 a new model for dissecting the mechanism of HSV-1 entry into the host.

195 able more rapid and complex modifications of HSV-1 and other large DNA viruses than previous technolo

196 immune response and in vivo pathogenesis of HSV-1 0DeltaNLS relative to its fully virulent parental

197 Propagation of HSV-1 on DHCR24(-/-) fibroblasts, which lack the desmost

198 playing the four essential entry proteins of HSV-1 and showed that they are capable of cell entry and

199 ne of the most abundant tegument proteins of HSV-1, but a well-established function has yet to be fou

200 ge was used to localize internal proteins of HSV-1, yielding insights into how capsid maturation is r

201 mine was ineffective in reducing the rate of HSV-1 reactivation in latently HSV-1-infected IFN-gamma-

202 s, play important roles in the regulation of HSV-1 fusion in the context of infection.

203 cosylation is important to the regulation of HSV-1-induced membrane fusion since mutating N58 to alan

204 minus of gK contributed to the regulation of HSV-1-induced membrane fusion.

205 T cells might not be the major regulators of HSV-1 latency in the mouse TG.

206 , AAV2 efficiently blocks the replication of HSV-1, which would eventually limit its own replication

207 ese results help explain how reproduction of HSV-1, a ubiquitous, medically significant human pathoge

208 The route of HSV-1 entry into keratinocytes has been the subject of l

209 models has demonstrated that the severity of HSV-1 ocular disease is influenced by three main factors

210 ne marks around transcription start sites of HSV-1-induced and constitutively transcribed antisense t

211 The viral dose with the McKrae strain of HSV-1 affected the level of viral DNA and time to explan

212 esults suggest that the avirulent strains of HSV-1, even after corneal scarification, had lower virus

213 es in neuronal spread between two strains of HSV-1.

214 time to reactivate than virulent strains of HSV-1.

215 Here, we report the crystal structure of HSV-1 UL37N.

216 The success of HSV-1 is largely due to its ability to establish lifelon

217 tropic determinants in the amino terminus of HSV-1 glycoprotein K (gK).

218 terns of disorder in Nbs1 reversed titers of HSV-1 produced in the cell.

219 Three-hour treatment of HSV-1 virions with pH 5 or multiple sequential treatment

220 Treatment of HSV-1-infected Vero cells with methyl beta-cyclodextrin

221 e structure and function of not just UL16 of HSV-1 but also its homologs in other herpesviruses.

222 tion mutations and to construct an oncolytic HSV-1 that utilizes the disialoganglioside GD2 as a HSV-

223 a potential alternative therapy in not only HSV-1 but also other conditions in which GODZ processing

224 assays demonstrated that UL20, but no other HSV-1 gene-encoded proteins, binds specifically to GODZ

225 y, low Rep protein levels in G1 phase permit HSV-1 replication but are insufficient for AAV2 replicat

226 ) T cells play a critical role in preventing HSV-1 reactivation from TG and subsequent virus shedding

227 ronal cells are able to support a productive HSV-1 infection, with kinetics and overall titers simila

228 stress-related hormones modulate productive HSV-1 and HSV-2 infections within sensory and autonomic

229 he impact of low-energy stress on productive HSV-1 growth and viral genetic determinants potentially

230 These results suggest that CTCF promotes HSV-1 lytic transcription by facilitating the elongation

231 Recombinant HSV-1 containing the ch14.18 single chain variable fragm

232 Here we report that recombinant HSV-1 with a mutation in the gamma134.5 protein, a virul

233 t and an inhibitor of palmitoylation reduced HSV-1 titers and altered the localization of UL20 and gl

234 egative GODZ construct significantly reduced HSV-1 replication in vitro and affected the localization

235 nstrate a novel approach to further reducing HSV-1 replication in the eye and latency in the TG by mo

236 ights into how UL20 palmitoylation regulates HSV-1 infectivity.IMPORTANCE HSV-1 UL20 is a nonglycosyl

237 This is difficult in humans, but mice show HSV-1 entry via the nose and then spread to its preferre

238 release, as well as the diffusion of single HSV-1 particles.

239 showed for the first time that HVEM-specific HSV-1 neutralizing antibodies protect mice from HSV-1 ey

240 of ICP0, a key viral protein that stimulates HSV-1 gene expression and replication.

241 interferon acting on myeloid cells can stop HSV-1 spread, and enhancing this defense offers a way to

242 nd peritoneal macrophages (PM) on subsequent HSV-1 infection.

243 These results demonstrated that HSV-1 infection induces the formation of channels penetr

244 We provide evidence that HSV-1 uses this to downregulate a strong inducer of apop

245 We have now identified that HSV-1 pUL7 and pUL51 form a stable and direct protein-pr

246 Our data show that HSV-1 0DeltaNLS lacks neurovirulence even in highly immu

247 Here, we show that HSV-1 induces the expression of about 1000 antisense tra

248 This study shows that HSV-1 can replicate without UL21, although the virus tit

249 The HSV-1 genome encodes numerous proteins that are dedicate

250 The HSV-1 virion protein 13/14 (VP13/14), also known as UL47

251 The HSV-1-encoded tegument protein UL16 is involved in multi

252 s, while not significantly influenced by the HSV-1 UL46-encoded phosphatidylinositol 3-kinase (PI3K)-

253 as used to clone 11 fragments comprising the HSV-1 strain KOS 152 kb genome.

254 g that cell cholesterol is important for the HSV-1 replicative cycle at a stage(s) beyond entry, afte

255 specific to three epitopes derived from the HSV-1 tegument protein VP13/14 (VP13/14286-294,VP13/1450

256 CTCF is known to bind several sites in the HSV-1 genome during latency and reactivation, but its fu

257 uggest multiple roles for cholesterol in the HSV-1 replicative cycle.IMPORTANCE HSV-1 infections are

258 s support the translational viability of the HSV-1 0DeltaNLS vaccine strain by demonstrating that, wh

259 The removal of the HSV-1 entry receptor Nectin-1 from the surface of the in

260 For instance, replication of the HSV-1 genome produces X- and Y-branched structures, remi

261 target for deletion of DNA sequences of the HSV-1 genome that span the region directing expression o

262 re we show that the C-terminal region of the HSV-1 pUL25 protein is required for releasing the viral

263 promoter into the VC2 vector in place of the HSV-1 thymidine kinase (UL23) gene.

264 These findings suggest that the HSV-1 LAT locus interferes with the host cellular immune

265 We found that the HSV-1 UL46 protein interacts with and colocalizes with S

266 Here, we establish that the HSV-1 Us3 protein kinase subverts the normal response to

267 Overall, the data suggest that the HSV-1 VC2 vaccine strain may be used as a viral vector f

268 novel immune evasion mechanism by which the HSV-1 LAT may contribute to the shaping of a broader rep

269 ort that CTCF interacts extensively with the HSV-1 DNA during lytic infection by ChIP-seq, and its kn

270 This HSV-1 mutant was able to replicate in noncomplementing c

271 y of human corneal epithelial (HCE) cells to HSV-1 infection, we infected HCE cells at three differen

272 or IL-36gamma, succumbed more frequently to HSV-1 infection than wild type mice.

273 ptive transfer of these stabilized iTregs to HSV-1-infected mice prevented the development of stromal

274 Reactivities to HSV-1 IgG, cytomegalovirus IgM, or cytomegalovirus IgG d

275 role during an intrinsic immune response to HSV-1 and are also degraded or inactivated by ICP0, here

276 strongly dampened the antiviral response to HSV-1 and the related virus Epstein-Barr virus (EBV), as

277 lood CD8 T cells and extended our studies to HSV-1.

278 We conclude that transient HSV-1 corneal infections cause long-term alterations of

279 Here, low-pH-treated HSV-1 was defective in fusion activity and yet retained

280 e rapidly than cells infected with wild-type HSV-1.

281 Unexpectedly, HSV-1 lytic genes, usually identified during acute infec

282 Additionally, UV-HSV-1 stimulates glycolysis and fatty acid oxidation-dep

283 at T cell-depleted human PBMCs exposed to UV-HSV-1 provide a survival benefit in a murine xenograft m

284 es, we typically infect mice with a virulent HSV-1 strain (McKrae) that does not require corneal scar

285 latently infected with avirulent or virulent HSV-1.

286 portant for control of herpes simplex virus (HSV-1) in the central nervous system (CNS).

287 This correlated with the time at which HSV-1 genome and mRNA levels in primary skin lesions sta

288 ng a well-established murine model, in which HSV-1 reactivation in latently infected trigeminal gangl

289 ing a well-established murine model in which HSV-1 reactivation was induced from latently infected TG

290 lmost exclusively in S/G2-phase cells, while HSV-1 DNA replication is restricted to G1 phase.

291 wed that C57BL/6 mouse corneas infected with HSV-1 KOS, which induces transient herpes epithelial ker

292 r lytic genes in cells or mice infected with HSV-1.

293 ying that in vivo cellular co-infection with HSV-1 and HSV-2 yields viable interspecies recombinants

294 Infection with HSV-1 induced relocalization of RNA5SP141 from the nucle

295 1 (CSF-1) DNA prior to ocular infection with HSV-1.

296 r infection following corneal infection with HSV-1.

297 then challenged by corneal inoculation with HSV-1 had reduced eye disease, shedding, and latent infe

298 nes and chemokines than M2 macrophages, with HSV-1 infection significantly increasing the levels of p

299 a model of peripheral infection of mice with HSV-1, we have characterized for the first time the neur

300 nal infection was incident or prevalent with HSV-1 or HSV-2 to generate annual numbers of incident ne