ライフサイエンスコーパス: HSV

1 HSV infection in these cultured cells shows the properti

2 HSV infects cells via multiple pathways, including a low

3 HSV mutants lacking both gE and US9 fail to properly ass

4 HSV type 1 (HSV-1) is a prevalent human pathogen that in

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

6 HSV-1 establishes latency within sensory neurons of trig

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

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

9 HSV-2 and T. pallidum were detected by serum antibody te

10 HSV-2 serostatus was assessed at baseline, at study exit

11 HSV-specific memory CD8(+) T cells play a critical role

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 uch as human herpes simplex virus 1 (HSV-1), HSV-2, and veterinarian pseudorabies virus (PRV), that i

45 herpes simplex virus types 1 (HSV-1) and 2 (HSV-2), and varicella zoster virus (VZV) by weekly polym

46 Barr virus (EBV), and herpes simplexvirus-2 (HSV-2).

47 rpes simplex virus type 1 (HSV-1) or type 2 (HSV-2) genital infection.

48 HIV and herpes simplex virus type 2 (HSV-2) infections cause a substantial global disease bur

49 Herpes simplex virus type 2 (HSV-2; herpes) exacerbates human immunodeficiency virus

50 l vaginosis and herpes simplex virus type-2 (HSV-2) infection.

51 All 3 HSV studies concluded that both sodium hypochlorite and

52 Of 365 HSV-2-seronegative persons, 68 acquired HSV-2, with 24 r

53 We identified 85 HSV-2 SNPs that, in aggregate, could determine whether p

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

55 365 HSV-2-seronegative persons, 68 acquired HSV-2, with 24 receiving TDF-containing ART and 44 recei

56 ional studies involving subjects with active HSV-2-specific immune responses.

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

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

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

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

61 patients deferred from testing truly had an HSV CNS infection.

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

63 Intralesional virotherapy with an HSV vector expressing GM-CSF has been recently approved

64 ns retaining sequences we posit as ancestral HSV-2.

65 We applied previous estimates of HSV-1 and HSV-2 prevalence and incidence in women aged 15-49 years

66 potential to differentially impact HSV-1 and HSV-2 so as to produce divergent outcomes of infection.

67 showed high effectiveness against HSV-1 and HSV-2 viruses, as found using a variety of techniques.

68 in vivo cellular co-infection with HSV-1 and HSV-2 yields viable interspecies recombinants in the nat

69 lexviruses, herpes simplex virus (HSV)-1 and HSV-2, with estimated divergence 6-8 million years ago (

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

71 ffective disinfection against adenovirus and HSV, the viruses commonly associated with nosocomial out

72 ties (PFU per viral genome) of HSV(chol) and HSV(des) were similar, suggesting cholesterol and desmos

73 o regulate internalization of KSHV, EBV, and HSV-2 in hematopoietic and endothelial cells.

74 tivation in latently HSV-1-infected mice and HSV-2-infected guinea pigs.

75 AP-HSV showed impaired vasomotor function that was associat

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

77 n that has been correlated with asymptomatic HSV-2 disease.

78 The average HSV PCR test turnaround time for the postimplementation

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

80 ystematic reviews of the association between HSV-2 and HIV found evidence that HSV-2 infection increa

81 al studies exploring the association between HSV-2 and HIV.

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

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

84 ell surface expression of CCR10 and CXCR3 by HSV-specific CD8 T cells compared to CD8 T cells specifi

85 The IFN response induced by HSV-2 was particularly dependent on IFI16.

86 man cervicovaginal histocultures infected by HSV-2 and in vivo in mice infected with RSV.

87 were susceptible to secondary infections by HSV-1.

88 SL), is selectively expressed on circulating HSV-2-specific CD8 T cells.

89 us-specific T cells are important to control HSV, and proliferation of activated T cells requires inc

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

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

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

93 roposed and validated criteria for deferring HSV PCR testing of CSF in immunocompetent hosts with nor

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

95 This study assessed the impact of a direct HSV (dHSV) PCR assay on the time to result reporting and

96 d specimens confirmed shedding of 2 distinct HSV-2 strains collected at different times in 17 pairs,

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

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

99 regulate transcription of type I IFNs during HSV infection.

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

101 hat protects peripheral nerve systems during HSV reactivation.

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

103 hlorite and 70% isopropyl alcohol eliminated HSV.

104 uggest that activation of TBK1 by engineered HSV is crucial for DC maturation, which may contribute t

105 if they assessed the effect of pre-existing HSV-2 infection on HIV acquisition; and if they determin

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

107 vaccine (formaldehyde-inactivated HSV-2 [FI-HSV-2]).

108 We further established that FI-HSV-2 alone or in combination with adjuvants as well as

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

110 ) is one of four glycoproteins essential for HSV entry and cell fusion.

111 The long-term outcomes with PPK for HSV keratitis in children provide improvement in BCVA wh

112 rst identified as a viral entry receptor for HSV, it is only recently that HVEM has emerged as an imp

113 VEM are the two major cellular receptors for HSV.

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

115 Adoption of criteria to screen for HSV test need proved cost-effective when less than 1 in

116 ment antigen targeted by CD8(+) T cells from HSV-seropositive individuals.

117 -1 neutralizing antibodies protect mice from HSV-1 eye disease, indicating the critical role of HVEM

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

119 Compared with baseline, genital HSV-2 shedding rates immediately after dosing were reduc

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

121 of 30 microg and 100 microg reduced genital HSV shedding and lesion rates.

122 lso eliminated glia with ganciclovir in Gfap(HSV-TK) mice.

123 ondii, which inhibited neither uptake of GFP-HSV nor localization of TLR9 in CD71(+) endosomes, direc

124 rior studies, none of the deferred cases had HSV encephalitis (n = 3120).

125 not CD8, T-cell phenotypes differed in HIV+/HSV-2+ versus HIV+/HSV-2- (overall P = .002) with increa

126 enotypes differed in HIV+/HSV-2+ versus HIV+/HSV-2- (overall P = .002) with increased frequency of CC

127 How HSV evolves within an infected individual experiencing m

128 biopsies obtained during asymptomatic human HSV-2 reactivation exhibit a higher density of nerve fib

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

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

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

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

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

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

135 ine IL-17c pretreatment reduced apoptosis in HSV-2-infected primary neurons.

136 zed to validate these metabolomic changes in HSV and to determine the efficacy of an improved prepara

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

138 a complete abrogation of NK cell function in HSV-2 infection.

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

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

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

142 h and without HIV infection participating in HSV-2 natural history studies (University of Washington

143 c nervous system plays a substantial role in HSV pathogenesis.

144 ated-virus vaccine (formaldehyde-inactivated HSV-2 [FI-HSV-2]).

145 he association between prevalent or incident HSV-2 infection and HIV seroconversion.

146 Following orofacial infection, HSV establishes latency in innervating sensory neurons,

147 2 phase support AAV2 replication and inhibit HSV-1 replication.

148 of herpes simplex virus 1 thymidine kinase (HSV-TK).

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

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

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

152 cosal immunology in ACB women and microbiome-HSV-2 interactions.

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

154 ates of genital HSV-1 infection and moderate HSV-2 prevalence meant the Americas had the highest over

155 ty profile in animal models of UL40, a novel HSV-2 T cell antigen that has been correlated with asymp

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

157 host factor in immunopathogenesis of ocular HSV type 1 (HSV-1) infection.

158 Subsequent analyses of HSV-infected cells by immunogold electron microscopy and

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

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

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

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

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

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

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

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

167 on between primary and recurrent episodes of HSV-2 infection and imply that strong selection pressure

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

169 A central feature of HSV pathogenesis is the ability to periodically reactiva

170 ific infectivities (PFU per viral genome) of HSV(chol) and HSV(des) were similar, suggesting choleste

171 ranched structures that are the hallmarks of HSV replication.

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

173 , even though evidence for the importance of HSV-2 antigen-specific CD8 T cells is mounting in animal

174 t and mechanism(s) of low-pH inactivation of HSV are unclear.

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

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

177 terone significantly decreased the levels of HSV-2 DNA replication and production of viral progeny in

178 servoir in the guinea pig challenge model of HSV-2 infection.

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

180 The presence of HSV-2 in a lesion was associated with presumed bacterial

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

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

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

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

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

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

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

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

189 ed to be infected with more than 1 strain of HSV-2 if their samples differed by >/=5 SNPs between the

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

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

192 of human origin would facilitate studies of HSV and other neurotropic viruses.

193 tion on keratinocytes, the initial target of HSV replication, to better understand this observation.

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

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

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

197 We measured cell surface ChR on HSV-specific human peripheral blood CD8 T cells and exte

198 ion in cell cultures, but a recent report on HSV-2 challenges those findings.

199 ceptors, CXCR3 and CCR10, are upregulated on HSV-specific CD8 T cells in blood.

200 proteins do not appear to be important once HSV is inside axons.

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

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

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

204 in aggregate, could determine whether paired HSV-2 strains were the same or different with >90% proba

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

206 rials Network 039 and Partners in Prevention HSV/HIV Transmission Study) in the US, Africa, and Peru

207 Productive HSV infection colocalized with these receptors in SCG bu

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

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

210 gation suggests that implementation of rapid HSV PCR testing can decrease turnaround times and the du

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

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

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

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

215 taining antiretroviral therapy (ART) reduces HSV-2 acquisition is unknown.

216 The adoption of criteria to screen HSV PCR tests in CSF represents a cost-effective approac

217 luate the adoption of criteria for screening HSV tests of CSF.

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

219 exhibited T cell responses against specific HSV-2 antigens not observed in symptomatic individuals.

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

221 evels of SEC-P-TEFb also potently stimulated HSV reactivation from latency both in a sensory ganglia

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

223 ession of a dominant-negative GluN1 subunit (HSV-dnGluN1) in VTA neurons to study the effect of trans

224 aining ART and 44 receiving ART without TDF (HSV-2 seroconversion incidence, 6.42 and 6.63 cases/100

225 ing that gE/gI and US9 function by tethering HSV particles to kinesin microtubule motors.

226 HSV-1 contributed more cases than HSV-2 in the Americas, Europe, and Western Pacific.

227 on between HSV-2 and HIV found evidence that HSV-2 infection increases the risk of HIV acquisition, b

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

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

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

231 The HSV membrane proteins gE/gI and US9 initiate the process

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

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

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

235 s in cocaine self-administering animals, the HSV-dnGluN1 treatment resulted in increased membrane lev

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

237 HIV acquisition; and if they determined the HSV-2 infection status of study participants with a type

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

239 As was done for the HSV-2 study, a UL21-null virus was made and propagated o

240 uggesting cholesterol and desmosterol in the HSV envelope support similar levels of infectivity.

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

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

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

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

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

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

247 Each of the HSV-2 genome sequences was initially obtained using next

248 ledge, new insights into the dynamics of the HSV-GAG interaction.

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

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

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

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

253 At the same time, HSV and PRV homologs cannot be swapped, which suggests t

254 against infection, as well as antibodies to HSV.

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

256 s in bacterial communities may contribute to HSV-2 ulcer pathogenesis, severity, or prolonged healing

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

258 ndicate that naturally occurring immunity to HSV-2 may be protective against infection with a second

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

260 crossover followed by back-recombination to HSV-2.

261 -alpha and TNF-alpha produced in response to HSV and HIV, thus functionally inactivating pDC.

262 y of roles in modulating immune responses to HSV and other pathogens, and there is increasing evidenc

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

264 r, this resulted in higher susceptibility to HSV-2 infection.

265 nocytes, their NK cells were unresponsive to HSV-2 challenge.

266 This study opens up a new avenue in treating HSV-induced SK lesions by increasing the stability and f

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

268 vels of IFI16 and induced more IFN-beta upon HSV-2 infection.

269 tive manner in ex vivo human saphenous vein (HSV) model.

270 e conducted this test using transient viral (HSV) expression of dominant-negative CaMKII-alpha (K42M)

271 eration of infectious extracellular virions (HSV(des)) that lack cholesterol and likely contain desmo

272 e adenovirus 8 and 19, herpes simplex virus (HSV) 1 and 2, human immunodeficiency virus 1, hepatitis

273 ses in vitroIMPORTANCE Herpes simplex virus (HSV) affects millions of people worldwide, causing painf

274 on specific.IMPORTANCE Herpes simplex virus (HSV) and other alphaherpesviruses, such as varicella-zos

275 tor (HVEM) facilitates herpes simplex virus (HSV) entry through interactions with a viral envelope gl

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

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

278 The terminase of herpes simplex virus (HSV) is composed of three subunits encoded by UL15, UL28

279 humor was positive for herpes simplex virus (HSV) or varicella zoster virus (VZV) in 79% to 100% of c

280 rabies virus (PRV) and herpes simplex virus (HSV) particles in living cells.

281 Despite frequent herpes simplex virus (HSV) reactivation, peripheral nerve destruction and sens

282 The herpes simplex virus (HSV) type I alkaline nuclease, UL12, has 5'-to-3' exonuc

283 sence of CMV, EBV, and herpes simplex virus (HSV) were independent predictors of genital HIV RNA shed

284 ies of simplexviruses, herpes simplex virus (HSV)-1 and HSV-2, with estimated divergence 6-8 million

285 In herpes simplex virus (HSV)-infected cells, ND10 bodies assemble at the sites o

286 FU ratio in vitro than herpes simplex virus (HSV).

287 RTANCE Infections by herpes simplex viruses (HSV) cause painful cold sores or genital lesions in many

288 ted women on antiretroviral therapy who were HSV-2 seropositive or seronegative and HIV-uninfected co

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

290 vical CD4+ T-cell number was associated with HSV-2 infection and a distinct cytokine profile.

291 After infection of primary cells with HSV or CMV, or transient transfection with naked plasmid

292 for management of individuals diagnosed with HSV-2 infection, particularly for those who are newly in

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

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

295 Ocular infection with HSV causes a chronic T cell-mediated inflammatory lesion

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

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

298 1 (CSF-1) DNA prior to ocular infection with HSV-1.

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

300 ned by an initial >457 basepair (bp) HSV-1 x HSV-2 crossover followed by back-recombination to HSV-2.