ライフサイエンスコーパス: HSV-2

1 aracterized for herpes simplex virus type 2 (HSV-2).

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

3 annually roughly (4000 for HSV-1; 10 000 for HSV-2).

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

5 reflect preexisting variation in circulating HSV-2.

6 ons in asymptomatic persons seropositive for HSV-2.

7 tive method for heterosexual transmission of HSV-2.

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

9 sensitivity of 87.1% for HSV-1 and 84.5% for HSV-2.

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

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

12 human herpesviruses (HHVs), including HHV-2 (HSV-2), a common human immunodeficiency virus (HIV)-1 co

13 pes simplex virus type 2 (HSV-2) and reduced HSV-2 acquisition as preexposure prophylaxis.

14 gel, an antiviral microbicide, in preventing HSV-2 acquisition in a subgroup of 422 HSV-2-negative wo

15 icoital application of tenofovir gel reduced HSV-2 acquisition in women.

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

17 HSV-2 acquisition was not reduced in HIV-infected, HSV-2

18 In contrast to effects on HSV-2 acquisition, tenofovir is unlikely to provide clin

19 creased risk of herpes simplex virus type 2 (HSV-2) acquisition in HIV pre-exposure prophylaxis trial

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

21 ich may contribute to the high prevalence of HSV-2 and early acquisition among African women.

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

23 tial impact on two epidemics, i.e., both the HSV-2 and HIV-1 epidemics.

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

25 diverse molecules for the prevention of HIV, HSV-2 and HPV acquisition, as well as unintended pregnan

26 reated cotton rat Sigmodon hispidus model of HSV-2 and HSV-1 genital infection.

27 ith and without condom use among 911 African HSV-2 and human immunodeficiency virus type 1 (HIV-1) se

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

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

30 implirix (gD/AS04) to protect humans against HSV-2 and the surprising finding that the vaccine protec

31 m clinically detected ulcers were tested for HSV-2 and Treponema pallidum by polymerase chain reactio

32 ctivity against herpes simplex virus type 2 (HSV-2) and reduced HSV-2 acquisition as preexposure prop

33 erpes simplex virus types 1 and 2 (HSV-1 and HSV-2), and cytomegalovirus were measured.

34 and HSV-2), carrageenan (CG; targets HPV and HSV-2), and levonorgestrel (LNG; targets unintended preg

35 de are infected with herpes simplex virus 2 (HSV-2), and to date, an efficacious prophylactic vaccine

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

37 ously reduces their risk of acquiring HIV-1, HSV-2, and HPV (latter two associated with increased ris

38 and in vivo were active against HIV-1ADA-M, HSV-2, and HPV16 PsV in cell-based assays.

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

40 Viremia with CMV, EBV, HHV-6, HSV-1, HSV-2, and VZV was detected in 60 (18%), 157 (48%), 80 (

41 er emulsion promoted most robust, functional HSV-2 antigen-specific CD8 T cell responses and high tit

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

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

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

45 Herpes simplex virus (HSV)-1 and HSV-2 are significant human pathogens causing recurrent

46 cells infected with herpes simplex virus 2 (HSV-2) are disrupted in their ability to form stress gra

47 erpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are important causes of acute neurologic illness.

48 an herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) are large DNA viruses associated with recurring o

49 an herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) are large-genome DNA viruses that establish a per

50 ity to EBV-viral capsid antigen and HSV-1 or HSV-2 (as indicators of recent infection) were 2.16 (95%

51 We evaluated genital ulcer disease (GUD) and HSV-2-associated GUD at quarterly visits or when spontan

52 ion (IRR, 1.83;P= .03), and the incidence of HSV-2-associated GUD increased from 8.1 to 19.0 episodes

53 We focused on herpes simplex virus type 2 (HSV-2) because prior published data have suggested a pos

54 suppresses HIV-1 ex vivo in tissues free of HSV-2 but endogenously coinfected with other HHVs.

55 HIV-1), zinc acetate (ZA; targets HIV-1 and HSV-2), carrageenan (CG; targets HPV and HSV-2), and lev

56 Incident HSV-2 cases were identified by evidence of seroconversio

57 onse to virus-driven inflammation.IMPORTANCE HSV-2 causes very localized recurrent infections in the

58 After intravaginal HSV-2 challenge, the mock and UL19/UL47 adenovirus group

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

60 of viral shedding in the genital tract after HSV-2 challenge.

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

62 educed plasma HIV-1 viral load (VL) in HIV-1/HSV-2 coinfected persons, and this was proposed to be du

63 ously reported at monthly visits in 3381 HIV/HSV-2-coinfected individuals in a placebo-controlled tri

64 nhanced HIV-1 infection and dissemination in HSV-2-coinfected mice.

65 to draining lymph nodes was detected only in HSV-2-coinfected mice.

66 Initiation of ART in HIV/HSV-2-coinfected persons is associated with a transient

67 y hCD4/R5/cT1 mice vaginally coinfected with HSV-2 could be completely prevented in almost half the m

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

69 ained genital swab specimens twice daily for HSV-2 detection and monitored genital lesions for 28-day

70 Whether tenofovir has utility in established HSV-2 disease is unclear.

71 Though HSV-2 disease is usually mild, it can be life threatenin

72 latory and effector T cells influences human HSV-2 disease.

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

74 iation of herpes simplex virus 1 (HSV-1) and HSV-2 DNA in 1,351 cutaneous and mucocutaneous specimens

75 low lesion scores, and a reduction in latent HSV-2 DNA in dorsal root ganglia to undetectable levels.

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

77 ssess factors associated with cervicovaginal HSV-2 DNA shedding and genital ulcer disease (GUD) in a

78 Cervicovaginal HSV-2 DNA was detected in 42% of women (99 of 236) in 8.

79 tion of genital disease, vaginal shedding of HSV-2 DNA, and latent infection of dorsal root ganglia i

80 articipants were screened for cervicovaginal HSV-2 DNA, GUD, cervicovaginal and systemic HIV-1 RNA, a

81 l genotyping, we estimated the prevalence of HSV-2 dual-strain infection and identified risk factors.

82 HSV-2 dual-strain infection was detected in 3.7% of pair

83 sed primarily on glycoproteins necessary for HSV-2 entry as target antigens and to which the dominant

84 These results are interpreted in light of HSV-2 evolution, epidemiology, and pathogenesis.

85 data provide no evidence for an influence of HSV-2 exposure on fibroid risk in young African-American

86 s explained by risk group, world region, and HSV-2 exposure type (prevalent vs incident).

87 ic neurons that become infected by HSV-1 and HSV-2 express stress hormone receptors and are responsiv

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

89 involving intramuscular (i.m.) injection of HSV-2 gB and gD in adjuvants have not been effective.

90 The HSV-2 gC2 and gD2 proteins were expressed in baculovirus

91 s a candidate therapeutic vaccine containing HSV-2 gD2TMR and ICP4.2, and Matrix-M2 adjuvant.

92 evac Trial for Women who experienced primary HSV-2 genital disease and compared them with sequences o

93 protected animals against HSV-1 compared to HSV-2 genital disease.

94 f HSV-1 genital herpes was less than that of HSV-2 genital herpes in cotton rats, and yet the model a

95 a microbicide, is an effective suppressor of HSV-2 genital infection in female BALB/c mice.

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

97 e-mediating mutations were identified in the HSV-2 genome at 3 loci in the UL5 gene and 1 locus in UL

98 isolates.IMPORTANCE The extent to which the HSV-2 genome evolves during multiple episodes of reactiv

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

100 However, only two full-length HSV-2 genomes have been reported.

101 mbination analysis was performed on multiple HSV-2 genomes.

102 Here we present six nearly complete HSV-2 genomic sequences, and, with the addition of two p

103 accines based on the herpes simplex virus 2 (HSV-2) glycoprotein D (gD-2) have been the major focus o

104 Up to 12 HSV-1 and HSV-2 glycoproteins are involved in HSV cell entry or ar

105 HSV-2 glycoproteins B (gB) and D (gD) are targets of neu

106 c vaccine containing herpes simplex virus 2 (HSV-2) glycoproteins C (gC2) and D (gD2) to stimulate hu

107 ociated with a transient increase in GUD and HSV-2 GUD.

108 We report that HSV-2 has a genomic overall mean distance of 0.2355%, wh

109 transmission of herpes simplex virus type 2 (HSV-2) has been examined in a variety of populations wit

110 long, recurrent genital infections caused by HSV-2 have failed.

111 c vaccines targeting herpes simplex virus 2 (HSV-2) have failed in the clinic to demonstrate sustaine

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

113 an antibody test to differentiate HSV-1 from HSV-2; however, this test has shown reduced capacity to

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

115 entified by evidence of seroconversion on an HSV-2 IgG enzyme-linked immunosorbent assay between stud

116 ) reactivity to EBV-viral capsid antigen and HSV-2 IgG, odds ratios were 2.16 (95% CI: 0.82, 5.70) an

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

118 e detection and differentiation of HSV-1 and HSV-2 in cutaneous and mucocutaneous swab specimens.

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

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

121 h prevalence of herpes simplex virus type 2 (HSV-2) in sub-Saharan Africa, the natural history of inf

122 influence of BV treatment on women's GUD and HSV-2 incidence and recurrence.

123 The HSV-2 incidence rate among the 25 women with vaginal ten

124 The HSV-2 incidence rate was 10.2 cases per 100 person-years

125 Herpes simplex virus 1 (HSV-1) and HSV-2 infect many humans and establish a latent infectio

126 Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) infect and establish latency in peripheral neuron

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

128 cytokine in the supernatant and also within HSV-2-infected MDDCs.

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

130 almost tripled in the presence of prevalent HSV-2 infection among general populations (adjusted RR 2

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

132 ses occurred in Africa, due to high maternal HSV-2 infection and high birth rates.

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

134 CD8 TRM cells in protection against genital HSV-2 infection and identify the population of APC that

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

136 To investigate whether HSV-2 infection directly facilitates mucosal HIV-1 acqui

137 entive antiviral medication for asymptomatic HSV-2 infection has benefit.

138 te that preformed SGs can be disassembled by HSV-2 infection in a manner that requires vhs endoribonu

139 nefits, and harms of serologic screening for HSV-2 infection in asymptomatic persons, including those

140 Incident HSV-2 infection in general populations was associated wi

141 Moreover, HSV-1 or HSV-2 infection in human cells blocked tumor necrosis fa

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

143 INTERPRETATION: We found evidence that HSV-2 infection increases the risk of HIV acquisition.

144 HSV-2 infection is a common cause of genital ulcer disea

145 his suggests that the genital microbiota and HSV-2 infection may influence HIV susceptibility through

146 Dynasore inhibited HSV-1 and HSV-2 infection of human epithelial and neuronal cells,

147 HSV-2 infection of isolated immature epidermal LCs, but

148 Stronger support for the causal effect of HSV-2 infection on BV risk was revealed by the summary r

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

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

151 HSV-2 infection stimulated local infiltration and activa

152 mized immunocompetent women with symptomatic HSV-2 infection to oral tenofovir disoproxil fumarate (T

153 Similar to HSV-1, HSV-2 infection triggered programmed necrosis in mouse c

154 V-2 infection, either at baseline (prevalent HSV-2 infection) or during follow-up (incident HSV-2 inf

155 V-2 infection) or during follow-up (incident HSV-2 infection).

156 ll' method confer protection against genital HSV-2 infection, and that IFN-gamma produced by CD8 TRM

157 he risk of HIV acquisition after exposure to HSV-2 infection, either at baseline (prevalent HSV-2 inf

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

159 igated the importance of basal autophagy for HSV-2 infection, using pharmacological autophagy suppres

160 HIV acquisition after prevalent or incident HSV-2 infection.

161 with valacyclovir for suppression of genital HSV-2 infection.

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

163 e to control local manifestations of primary HSV-2 infection.

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

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

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

167 Genital herpes simplex virus type 2 (HSV-2) infection causes recurrent lesions and frequent v

168 Globally, herpes simplex virus type 2 (HSV-2) infection is the most common cause of genital ulc

169 role of autophagy in Herpes simplex virus-2 (HSV-2) infection is unknown.

170 ect against one herpes simplex virus type 2 (HSV-2) infection protects against infection with additio

171 se to a mucosal herpes simplex virus type 2 (HSV-2) infection.

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

173 te disease symptoms resulting from HSV-1 and HSV-2 infections and is associated with the appearance o

174 sterone selectively modulate acute HSV-1 and HSV-2 infections in autonomic, but not sensory, neurons.

175 lated hormones modulate productive HSV-1 and HSV-2 infections within sensory and autonomic neurons, w

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

177 or treatment of herpes simplex virus type 2 (HSV-2) infections.

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

179 association with fibroids, and serology for HSV-2 is much more sensitive than self-report.

180 Herpes simplex virus 2 (HSV-2) is a causative agent of genital and neonatal herp

181 Herpes simplex virus 2 (HSV-2) is a major global pathogen, infecting 16% of peop

182 In one participant's HSV-2 isolate, we found a previously unidentified mutati

183 r results also demonstrate that some primary HSV-2 isolates from North America more closely resemble

184 e characterized mutations from 32 cultivated HSV-2 isolates previously found to be susceptible to pri

185 nclusion in future studies of North American HSV-2 isolates.IMPORTANCE The extent to which the HSV-2

186 The HSV-2 LAT and viral miRNAs expressed in the LAT region a

187 t the nearly complete genome sequences of 34 HSV-2 low-passage-number and laboratory strains, 14 of w

188 In this study, we sequenced 34 additional HSV-2 low-passage-number and laboratory viral genomes an

189 HSV-2 maintains a latent infection in sensory neurons an

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

191 cation are not related to the suppression of HSV-2-mediated inflammation and are consistent with a di

192 We previously reported an HSV-2 mutant, HSV2-gD27, in which the nectin-1 binding d

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

194 nting HSV-2 acquisition in a subgroup of 422 HSV-2-negative women enrolled in the Centre for the AIDS

195 it vaccine, despite inducing lower titers of HSV-2 neutralizing antibodies in the serum.

196 entry into human cells, but unlike HSV-1 and HSV-2, none of the clinical strains uses an HVEM-mediate

197 Transmission of HSV-2 occurred in 68 couples, including 17 with suscepti

198 a population of 100000 with a prevalence of HSV-2 of 16% (the seroprevalence in US adults with unkno

199 ed the effects of coinfection with HIV-1 and HSV-2 on monocyte-derived DCs (MDDC).

200 These studies tested the impact of HSV-2 on systemic T-cells and HIV reservoirs.

201 subsequently challenged intravaginally with HSV-2 or HSV-1.

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

203 ere detected at higher relative abundance in HSV-2 PCR-positive than negative ulcers.

204 eening tests were from populations with high HSV-2 prevalence (greater than 40% based on Western blot

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

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

207 f protein (vhs) as a herpes simplex virus 2 (HSV-2) protein capable of disrupting SG formation.

208 y and harms of serologic screening tests for HSV-2; RCTs assessing preventive interventions in asympt

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

210 reg (CD4(+)Foxp3(+)) population during human HSV-2 reactivation in situ in sequential genital skin bi

211 Keratinocytes produced IL-17c during HSV-2 reactivation, and IL-17RE, an IL-17c-specific rece

212 Herpes simplex virus type 2 (HSV-2) reactivation is accompanied by a sustained influx

213 Healthy adults with 4 to 9 annual genital HSV-2 recurrences were eligible.

214 herapy (ART) on herpes simplex virus type-2 (HSV-2) replication is unclear.

215 es of 95.7 and 97.6% for detecting HSV-1 and HSV-2, respectively.

216 used to assess relationships among the four HSV-2 samples, other North American sequences, and refer

217 comparable numbers of full-length HSV-1 and HSV-2 sequences enabled comparative analysis of gene div

218 This was the first study to analyze multiple HSV-2 sequences, and the data will be valuable in future

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

220 adults who were HSV-2 seropositive and 2 in HSV-2-serodiscordant couples.

221 96 participants, 1,658 had blood samples and HSV-2 serology results; 22% of participants with serolog

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

223 ether valACV suppresses VL in HIV-1 infected HSV-2-seronegative persons.

224 in nonpregnant asymptomatic adults who were HSV-2 seropositive and 2 in HSV-2-serodiscordant couples

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

226 Among 49 ulcer specimens from 49 HSV-2 seropositive women, by PCR HSV-2 was recovered fro

227 edding frequency and quantity are high among HSV-2-seropositive adults in sub-Saharan Africa, includi

228 genital skin biopsy specimens obtained from HSV-2-seropositive subjects at the time of lesion onset

229 Ninety-three HSV-2-seropositive Ugandan adults collected anogenital s

230 There was no significant association between HSV-2 seropositivity and the presence of fibroids (multi

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

232 Associations with HSV-2 shedding and quantity were examined using random-e

233 HSV-2 shedding frequency and quantity are high among HSV

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

235 HSV-2 shedding was lower among men with healed MC wounds

236 Detectable penile HSV-2 shedding was present in 9.7% of men (17 of 176) be

237 Of the 236 women with data on HSV-2 shedding, 151 took ART during the study period.

238 associated with a decrease in cervicovaginal HSV-2 shedding, and the impact was sustained over severa

239 ere coincident with a suppression of vaginal HSV-2 shedding, low lesion scores, and a reduction in la

240 s associated with a reduction in the odds of HSV-2 shedding, which declined for each year of ART use

241 With simultaneous coinfection, HSV-2 significantly stimulated HIV-1 DNA production 5-fo

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

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

244 In this study, circulating HSV-2-specific CD8 T cells were identified using specifi

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

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

247 the amount of genomic DNA variation between HSV-2 strains because only two genomes have been determi

248 Unexpectedly, we found that circulating HSV-2 strains can contain HSV-1 DNA segments in three di

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

250 resistance-mediating mutations, we analyzed HSV-2 strains detected in genital swab specimens from tr

251 itiated analysis of the genetic diversity of HSV-2 strains from around the world.

252 n protects against infection with additional HSV-2 strains is important for understanding the potenti

253 Extensive recombination between the HSV-2 strains was also strongly implied.

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

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

256 Interventions targeting HSV-2, such as new HSV vaccines, have the potential for

257 f receptors distinct from those for HSV-1 or HSV-2 suggests a possible mechanism of enhanced neuropat

258 Pharmacologic HSV-2 suppression may reduce BV incidence and BV-associa

259 y (ART) during a placebo-controlled trial of HSV-2 suppression with acyclovir in Rakai, Uganda.

260 Several trials demonstrated that HSV-2 suppressive therapy using ACV or its prodrug valac

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

262 However, its homolog in HSV-2, termed ICP27t2, has been little studied.

263 longer survival after vaginal challenge with HSV-2 than immunization with HPV-gBsec or HPV-gDsec alon

264 etter protection from vaginal challenge with HSV-2 than that obtained with a subunit vaccine, despite

265 Herpes simplex virus 2 (HSV-2), the principal causative agent of recurrent genit

266 ong adults with frequently recurring genital HSV-2, the use of pritelivir compared with valacyclovir

267 ess hormones are thought to impact HSV-1 and HSV-2 through immune system suppression, sensory and aut

268 There was a direct correlation between HSV-2 titer and Treg density.

269 tion was incident or prevalent with HSV-1 or HSV-2 to generate annual numbers of incident neonatal in

270 rates evidence of retained susceptibility of HSV-2 to pritelivir in immunocompetent persons following

271 ndoms were differentially protective against HSV-2 transmission by sex; condom use reduced per-act ri

272 e used to associate the log10 probability of HSV-2 transmission over monthly risk periods with report

273 We examined the per-act HSV-2 transmission rates with and without condom use amo

274 The strong HSV-2 trapping ability of ZOTEN significantly reduced th

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

276 acquisition was not reduced in HIV-infected, HSV-2-uninfected persons during TDF-containing ART.

277 men was tested for the presence of HSV-1 and HSV-2 using the illumigene assay, and results were compa

278 rotein D (gD-2) have been the major focus of HSV-2 vaccine development for the past 2 decades.

279 mportant for understanding the potential for HSV-2 vaccine development.

280 er, our data indicate that a live attenuated HSV-2 vaccine impaired for infection of neurons provides

281 her highlighted by the recent failure of GSK HSV-2 vaccine Simplirix (gD/AS04) to protect humans agai

282 ting mice with a new type of live attenuated HSV-2 vaccine that is impaired for infection of neurons

283 No herpes simplex virus 2 (HSV-2) vaccine has been licensed for use in humans.

284 cal and clinical development of prophylactic HSV-2 vaccines that contain appropriate antigen and adju

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

286 s lower in subpopulations of CD4+ T-cells in HSV-2+ versus HSV-2- women.

287 We analyzed the ability of HSV-2 vhs carrying the point mutation D215N, which ablat

288 el, ZOTEN promoted the presentation of bound HSV-2 virions to mucosal APCs, enhancing T cell-mediated

289 , we evaluated the efficacy and safety of an HSV-2 virus deleted in gD-2 and complemented allowing a

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

291 HSV-2 was detected from 2484 of 11 283 swab specimens co

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

293 ens from 49 HSV-2 seropositive women, by PCR HSV-2 was recovered from 28 (57%) specimens and T. palli

294 Detection of HSV-2 was similar, with a sensitivity of 98.9% and a spe

295 and 99.7%, respectively, for both HSV-1 and HSV-2, whereas ELVIS had a resolved sensitivity of 87.1%

296 biopsy specimens from persons with recurrent HSV-2, while the mRNA levels of the CCR10 ligand CCL27 w

297 365 HSV-2-seronegative persons, 68 acquired HSV-2, with 24 receiving TDF-containing ART and 44 recei

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

299 populations of CD4+ T-cells in HSV-2+ versus HSV-2- women.

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