ライフサイエンスコーパス: HSV-2

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

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

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

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

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

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

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

8 reflect preexisting variation in circulating HSV-2.

9 es postnatally with lethal doses of HSV-1 or HSV-2.

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

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

12 f effect of vaginal TFV 1% gel in preventing HSV-2 acquisition among women in VOICE, randomized, doub

13 nimal model to develop strategies to prevent HSV-2 acquisition and reactivation.

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

15 tenofovir (TFV) gel provided protection from HSV-2 acquisition in the CAPRISA 004 study.

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

17 od of 501 person-years, 92 incident cases of HSV-2 acquisition occurred: 77 were in women with no TFV

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

19 Of 566 participants at risk for HSV-2 acquisition, 532 (94%) had first-quarter plasma TF

20 ciated with a trend toward a reduced risk of HSV-2 acquisition, after controlling for sexual behavior

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

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

23 pathogens herpes simplex virus 1 (HSV-1) and HSV-2 and are significant causes of ulcerative mucosal s

24 thelium is the first line of defense against HSV-2 and coordinates the immune response through the se

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

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

27 Because HSV-2 and HIV have shared sexual and other risk factors,

28 Estimates were calculated by incorporating HSV-2 and HIV infection data with pooled relative risk (

29 systematically-assembled database for paired HSV-2 and HIV seroprevalence measures among FSWs.

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

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

32 Infectious HSV-2 and HSV-2 DNA were consistently shed in vaginal sw

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

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

35 HSV-1 and HSV-2 and other primate viruses within the Simplexvirus

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

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

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

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

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

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

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

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

44 HSV-2 antibody was detected in serum.

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

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

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

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

49 ions of interspecies recombination events in HSV-2 are significantly more variable than previously ap

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

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

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

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

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

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

56 We found that HSV-2 can infect RM after vaginal inoculation, establish

57 Herpes simplex virus 2 (HSV-2) can be transmitted in the presence or absence of

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

59 Using IL-36gamma(-/-) mice in a lethal HSV-2 challenge model, we show that neutrophil counts ar

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

61 vaginal cavity and protected against lethal HSV-2 challenge.

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

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

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

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

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

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

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

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

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

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

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

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

74 Further, HSV-2 DNA was detected in ganglia in most necropsied ani

75 Infectious HSV-2 and HSV-2 DNA were consistently shed in vaginal swabs for th

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

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

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

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

80 were based on eight recombinantly expressed HSV-2 envelope and tegument proteins.

81 [4.0-25.6]), living in Lome (2.8 [1.1-7.1]), HSV-2 excretion (26.7 [2.9-244.3]), C. trachomatis (11.7

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

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

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

85 Reactivation of herpes simplex virus 2 (HSV-2) from latency causes viral shedding that develops

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

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

88 oped an agent-based mathematical model of an HSV-2 genital ulcer to integrate mechanistic observation

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

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

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

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

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

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

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

96 However, HSV-2 has also been found latent in autonomic ganglia.

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

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

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

100 The study identified 231 paired HSV-2/HIV prevalence measures from 40 countries.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Notably, acyclovir did not eliminate HSV-2-induced HIV-1 reactivation.

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

118 his subset of immune cells was depleted from HSV-2-infected guinea pigs by injection of an anti-CD4 m

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

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

121 9 years (32.4% [25.4-40.2]), and established HSV-2 infection (26.8% [19.7-34.5]).

122 years, and 15-49 years), sex, and timing of HSV-2 infection (established vs recently acquired).

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

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

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

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

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

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

129 r of incident HIV infections attributable to HSV-2 infection by age (15-24 years, 25-49 years, and 15

130 New preventive interventions against HSV-2 infection could not only improve the quality of li

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

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

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

134 limb paralysis that is linked to productive HSV-2 infection in the brain stem.

135 ates many of the key features of subclinical HSV-2 infection in women but seems to be more limited, a

136 e features mimic some of the key features of HSV-2 infection in women.

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

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

139 interactions, an animal model of subclinical HSV-2 infection is needed.

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

141 Thus, HSV-2 infection of RM recapitulates many of the key feat

142 lative risk (RR) estimates for the effect of HSV-2 infection on HIV acquisition from a systematic rev

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

144 le to HSV-2 infection, even if the effect of HSV-2 infection on HIV had been imperfectly measured in

145 mitted diseases, with a global prevalence of HSV-2 infection predicted to be over 536 million worldwi

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

147 shedding using a guinea pig model of genital HSV-2 infection that recapitulates the shedding of virus

148 imed to assess the potential contribution of HSV-2 infection to HIV incidence, given an effect of HSV

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

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

151 ns are strongly associated with black males, HSV-2 infection, and other factors known to increase rat

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

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

154 urden of HIV is likely to be attributable to HSV-2 infection, even if the effect of HSV-2 infection o

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

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

157 ged 15-49 years in 2016 were attributable to HSV-2 infection.

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

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

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

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

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

163 fected cells and eradicate briskly spreading HSV-2 infection.

164 safe sustained-delivery platform to prevent HSV-2 infection.

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

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

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

168 ers, those with herpes simplex virus type 2 (HSV-2) infection, men who had sex at an early age, those

169 ndividuals with herpes simplex virus type 2 (HSV-2) infection.

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

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

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

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

174 As initial acquisition of both HIV and HSV-2 infections is subclinical, study of the initial mo

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

176 exerts antiviral activity against HSV-1 and HSV-2 infections.

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

178 oculation.IMPORTANCE Herpes simplex virus 2 (HSV-2) infects nearly 500 million persons globally, with

179 sed in cervical secretions immediately after HSV-2 inoculation.

180 To study host-HSV-2 interactions, an animal model of subclinical HSV-2

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

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

183 HSV-2 is a neurotropic virus that causes a persistent, l

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

185 contribute to viral pathogenesis.IMPORTANCE HSV-2 is a ubiquitous important human pathogen that caus

186 HSV-2 is associated with increased human immunodeficienc

187 tion is likely to be greatest in areas where HSV-2 is highly prevalent, particularly Africa.

188 Herpes simplex virus 2 (HSV-2) is a common sexually transmitted infection with a

189 infection with herpes simplex virus type 2 (HSV-2) is common and increases risk of human immunodefic

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

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

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

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

194 6A], HHV-6B, herpes simplex virus 1 [HSV-1], HSV-2, JC virus [JCV], and varicella-zoster virus [VZV])

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

196 29 vaccine, based on a replication-defective HSV-2 mutant virus, which has been recently tested in cl

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

198 l microenvironment and may function to limit HSV-2 neuroinvasion.

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

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

201 fection to HIV incidence, given an effect of HSV-2 on HIV acquisition.

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

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

204 ae, P = .03; Mycoplasma genitalium, P = .04; HSV-2, P = .001; and a trend for Chlamydia trachomatis,

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

206 nd/or G) at a total dose of 1 x 10(7) PFU of HSV-2 per animal.

207 CI 0.3-9.9%) among populations of FSWs with HSV-2 prevalence < 25% to 18.7% (95% CI 14.1-23.8%) amon

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

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

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

211 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

212 49%, to 13.4 (95% CI 6.1-29.9) in those with HSV-2 prevalence 75-100%.

213 o 18.7% (95% CI 14.1-23.8%) among those with HSV-2 prevalence 75-100%.

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

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

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

217 Out of the eight HSV-2 proteins, the envelope glycoprotein D (gD), the te

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

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

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

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

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

223 ting 90% of the global population, HSV-1 and HSV-2 represent some of the most prevalent viruses in th

224 2 shedding.IMPORTANCE Sexual transmission of HSV-2 results from viral shedding following reactivation

225 Reactivation of herpes simplex virus 2 (HSV-2) results in infection of epithelial cells at the n

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

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

228 ciated with a trend toward a reduced risk of HSV-2 seroconversion, with an unadjusted hazard ratio (H

229 ad first-quarter plasma TFV and end-of-study HSV-2 serologic data available.

230 96 participants, 1,658 had blood samples and HSV-2 serology results; 22% of participants with serolog

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

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

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

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

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

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

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

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

239 vaginal and penile microbiomes contribute to HSV-2 serostatus within sexual partnerships.

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

241 cell populations and mechanisms that control HSV-2 shedding are not well understood.

242 The cumulative number of HSV-2 shedding days and the mean number of days virus wa

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

244 demonstrated by the detection of spontaneous HSV-2 shedding post-acute inoculation (10(2) to 10(3) DN

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

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

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

248 e importance of CD4(+) T cells in control of HSV-2 shedding, this subset of immune cells was depleted

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

250 of therapeutic vaccines designed to control HSV-2 shedding.IMPORTANCE Sexual transmission of HSV-2 r

251 -2, completely protected mice from HSV-1 and HSV-2 skin or vaginal disease and prevented latency foll

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

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

254 HSV-2-specifc T-cell responses were detected in all anim

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

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

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

258 A sufficiently high density of HSV-2-specific Trm cells predicted rapid elimination of

259 esting that IL-36gamma may function to limit HSV-2 spread in the nervous system.

260 d penile taxa and covariates contributing to HSV-2 status in women and men using bivariate probit.

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

262 inoculated intravaginally with two or three HSV-2 strains (186, 333, and/or G) at a total dose of 1

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

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

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

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

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

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

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

270 HSV-2 surveillance could inform HIV preparedness in coun

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

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

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

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

275 The contribution of HSV-2 to HIV was largest for the WHO African region (PAF

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

277 aginal epithelium and a more rapid spread of HSV-2 to the spinal cord, bladder, and colon.

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

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

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

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

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

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

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

285 T, while herpes simpex virus 1 and 2 (HSV-1, HSV-2), varicella-zoster virus (VZV) and human herpesvir

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

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

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

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

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 Among 231 couples, HSV-2 was detected in: 78 (33.8%) both the man and woman

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

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

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

296 ected in all animals, although antibodies to HSV-2 were detected in only 30% of the animals.

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

298 365 HSV-2-seronegative persons, 68 acquired HSV-2, with 24 receiving TDF-containing ART and 44 recei

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

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

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