ライフサイエンスコーパス: latent infection

1 HSV-1 had reduced eye disease, shedding, and latent infection.

2 more than 150 lncRNAs between its active and latent infection.

3 HIV-1 genomes, and immunotherapies to clear latent infection.

4 RNA species may contribute significantly to latent infection.

5 he establishment of a life-long asymptomatic latent infection.

6 LANA) E3 ligase activity in gammaherpesvirus latent infection.

7 o the development of strategies to eliminate latent infection.

8 differentially expressed mRNAs in active and latent infection.

9 elease assay (QuantiFERON [QFT]) to test for latent infection.

10 iscriminated between active tuberculosis and latent infection.

11 e septicemia to chronic localized illness or latent infection.

12 e various cellular pathways to establish the latent infection.

13 phenotypically similar to that of wild-type latent infection.

14 viral cyclin that promotes reactivation from latent infection.

15 s one of the major proteins expressed during latent infection.

16 ive disease than in those that would develop latent infection.

17 that express viral microRNAs (miRNAs) during latent infection.

18 as linked to treatment for active disease or latent infection.

19 h the possibility to discriminate active and latent infection.

20 which activated NF-kappaB and promoted KSHV latent infection.

21 rant lytic gene expression and impaired KSHV latent infection.

22 s impact on host gene expression during KSHV latent infection.

23 arbor this virus allowing the persistence of latent infection.

24 to enable host NF-kappaB activation and KSHV latent infection.

25 ral gene expression and the establishment of latent infection.

26 IKKbeta and IKKepsilon that were crucial for latent infection.

27 ased KSHV lytic gene expression and impaired latent infection.

28 s share a remarkable propensity to establish latent infection.

29 HV has evolved with strategies to facilitate latent infection.

30 tion of infectious agents or reactivation of latent infection.

31 reduced gene expression under conditions of latent infection.

32 HIV infection, including both productive and latent infection.

33 on than disease resulting from activation of latent infection.

34 uberculosis (TB) and prevent reactivation of latent infection.

35 liminate the virus because HIV-1 establishes latent infection.

36 known which types of CD34(+) cells support a latent infection.

37 th positive skin tests risks underestimating latent infection.

38 ese treatments in preventing reactivation of latent infection.

39 PCR) homolog US28 is required for successful latent infection.

40 g from bacterial clearance to progressive or latent infection.

41 ent antiviral therapies target lytic but not latent infection.

42 n AP-1 binding to the MIEP, compared with WT latent infection.

43 levels similar to those we observe during WT latent infection.

44 ers for the experimental use of VOR to clear latent infection.

45 episomes inside the host cell nucleus during latent infection.

46 ymphocyte pool through a growth-transforming latent infection.

47 uman pathogens that switch between lytic and latent infection.

48 latency, none has demonstrated clearance of latent infection.

49 ssion which can lead to the establishment of latent infections.

50 rion-delivered genomes during both lytic and latent infections.

51 cterium tuberculosis (MTB) and in those with latent infections.

52 ocytes, and monocytes) to establish lifelong latent infections.

53 (HSV-1) is a key regulator in both lytic and latent infections.

54 ding the host immune system and establishing latent infections.

55 are human pathogens that establish lytic and latent infections.

56 examined so far appear to be associated with latent infections.

57 B lymphocyte signaling to achieve persistent latent infections.

58 , maintain, and reactivate HCMV experimental latent infections.

59 tral nervous system (CNS) but may exacerbate latent infections.

60 vantage of epigenetic silencing to establish latent infections.

61 a common beta-herpesvirus causing life-long latent infections.

62 as a divergence point between productive and latent infections.

63 s characteristic of reactivation of lifelong latent infections.

64 that may play roles in regulating lytic and latent infections.

65 In sensory neurons it establishes a silent (latent) infection.

66 During latent infection, a restricted gene expression program l

67 ate RelA in a site-specific manner to enable latent infection after KSHV de novo infection.

68 CG/H56-vaccinated monkeys did not reactivate latent infection after treatment with anti-TNF antibody.

69 latter have major clinical implications, as latent infection allows the virus to persist despite ant

70 he model suggests that a small proportion of latent infections among human immunodeficiency virus-pos

71 ulosis is classically divided into states of latent infection and active disease.

72 ated by difficulty in discriminating between latent infection and active disease.

73 tb bacteremia with progressive phenotypes of latent infection and active pulmonary tuberculosis.

74 Human herpesviruses (HHV) establish lifelong latent infection and are transmitted primarily via shedd

75 pes simplex virus (HSV) establishes lifelong latent infection and can cause serious human disease, bu

76 mallei to generate either acute, chronic, or latent infection and host blood and tissue transcription

77 and compared them to levels in patients with latent infection and normal glycemic control.

78 origin and new opportunities to inhibit EBV latent infection and pathogenesis.

79 It establishes a lifelong latent infection and persists in infected cells without

80 The establishment of latent infection and poorly characterized viral reservoi

81 environments for preventing reactivation of latent infection and possibly shortening the duration of

82 Evidence of latent infection and reactivation was demonstrated by th

83 cannot distinguish tuberculosis disease from latent infection and some lack specificity.

84 body profiles: early, transient responses in latent infection and stable antibody increase in active

85 The establishment of latent infection and subsequent reactivations, during wh

86 pisomes are prepared such that they maintain latent infection and switch to lytic replication by K-Rt

87 ynomolgus macaques develop active disease or latent infection and that latently infected animals reac

88 strategy to block the establishment of KSHV latent infection and the associated malignancies.

89 New insights into the mechanisms of latent infection and the importance of reservoirs of inf

90 provide insight into the maintenance of KSHV latent infection and the switch to lytic replication.

91 existing treatment can effectively eradicate latent infection and therefore a cure is lacking for man

92 It can stabilize HIF-1alpha during latent infection and undergoes lytic replication in resp

93 Both latent infection and viral protein expression contribute

94 LAcmvIL-10 (expressed during both lytic and latent infection) and cmvIL-10 (identified only during l

95 In cell culture, KSHV results in a latent infection, and lytic reactivation is usually indu

96 CMV, a herpesvirus that causes a persistent/latent infection, and vaccinia virus, a poxvirus that is

97 h the depleting MAb after establishment of a latent infection, and vaginal swabs were taken daily to

98 Latent infection appears to wane within the transitional

99 e genes that are differentially regulated in latent infection are occupied by LANA at their promoters

100 axons to peripheral ganglia, where life-long latent infections are established.

101 virus (EBV) can efficiently establish stable latent infection as a chromatinized episome in the nucle

102 Epstein-Barr virus (EBV) establishes latent infection as chromatin-assembled episomes in whic

103 Epstein-Barr virus (EBV) establishes latent infections as multicopy episomes with complex pat

104 tion of capillary-like tube formation during latent infection, as the addition of exogenous TGF-beta2

105 is sufficient to restrict M. tuberculosis to latent infection, but most infections are not completely

106 is expressed during latency and facilitates latent infection by attenuating the activator protein-1

107 Latent infection by Kaposi's sarcoma-associated herpesvi

108 actions in the ganglia during both acute and latent infection by measuring both viral and host transc

109 ted herpesvirus (KSHV) establishes life-long latent infection by persisting as an extra-chromosomal e

110 We demonstrate that in this model, latent infection can be established in all subsets of HP

111 Strategies to eradicate latent infection can only be evaluated with robust, sens

112 eurons in which they can establish a silent, latent infection characterized by the expression of a no

113 KSHV latent infection decreases mitochondrial numbers, but th

114 Thus, KG-1 and Kasumi-3 experimental latent infections differ in important parameters from th

115 he most highly expressed viral miRNAs during latent infection, directly targets the cellular receptor

116 For active disease and latent infection donors from two populations (London, U.

117 alent herpes virus causing lifelong, usually latent, infections, drives the expansion of the CD56(dim

118 fected cells, particularly those harboring a latent infection during which UL138 is one of the few vi

119 We do this by linking latent infection dynamics with a mechanistic model of an

120 During latent infection, EBV encodes latent membrane protein 2A

121 ion events; however, in some rare instances, latent infection events are established.

122 etermine whether HIV-1 establishes active or latent infection events remain largely elusive.

123 ynamics in resting naive T cells rescues HIV latent infection following CD3/CD28 stimulation.

124 t Mtb infection, as shown by reactivation of latent infection following simian immunodeficiency virus

125 variety of diseases, can establish lifelong latent infections from which virus can reactivate to cau

126 harmacological HIV-1 reactivation to reverse latent infection has been extensively studied.

127 latency, cell culture models of quiescent or latent infection have been developed.

128 Viral latent infections have numerous associated pathologies,

129 (i) a mechanism utilized by KSHV to maintain latent infection, (ii) a latency-lytic cycle switch oper

130 eant that the median number of children with latent infection in 2010 was 53,234,854 (41,111,669-68,9

131 EBV establishes latent infection in B cells, which is the typical progra

132 2 decades of life and establishes reversible latent infection in B cells.

133 in-Barr virus (EBV) establishes a persistent latent infection in B lymphocytes and is associated with

134 gion of the HCMV genome as important for the latent infection in CD34(+) hematopoietic progenitor cel

135 Existing as a latent infection in CD34(+) progenitors and circulating

136 bound viremia.IMPORTANCE HIV-1 persists as a latent infection in CD4(+) T cells that can be found in

137 nted through identification and treatment of latent infection in close collaboration with a pre-entry

138 ticus as well as the role of reactivation of latent infection in encephalitis following cord blood st

139 e virus was highly deficient in establishing latent infection in germinal center B cells.

140 Human cytomegalovirus (HCMV) can establish latent infection in hematopoietic progenitor cells (HPCs

141 on factor b (P-TEFb) in the establishment of latent infection in HPCs.

142 ted herpesvirus (KSHV) establishes long-term latent infection in humans and can cause cancers in endo

143 response could prevent CMV from establishing latent infection in humans and support the achievability

144 la-zoster virus (VZV) establishes a lifelong latent infection in humans following primary infection.

145 ed herpesvirus (KSHV) establishes persistent latent infection in immunocompetent hosts.

146 erpesviruses, HHV-6A establishes a lifelong, latent infection in its host.

147 erpesvirus (KSHV) that establishes acute and latent infection in laboratory mice.

148 virus Peru (RHVP) that establishes acute and latent infection in laboratory mice.

149 ary infection, HHV-6B persists as a chronic, latent infection in many cell types.

150 elial and lymphoid malignancies, establishes latent infection in memory B cells, and intermittently p

151 fferentiation process to establish life-long latent infection in memory B cells.

152 KSHV established latent infection in MM cells, and lytic induction result

153 uman malignancies and can establish lifelong latent infection in multiple cell types within its human

154 of human CMV (HCMV) to enter and establish a latent infection in myeloid cells is crucial for surviva

155 uripotency, plays a role in maintaining KSHV latent infection in naturally infected cells.

156 Herpes simplex virus-1 (HSV-1) establishes a latent infection in neurons and periodically reactivates

157 ubiquitous virus that establishes a lifelong latent infection in neurons.

158 mplex virus 1 (HSV-1) establishes a lifelong latent infection in peripheral nerve ganglia.

159 HSV-1 can also establish a more quiescent or latent infection in peripheral neurons, where gene expre

160 HSV can also establish a more quiescent or latent infection in peripheral neurons.

161 Establishment of a quiescent or latent infection in PNS neurons is a hallmark of most al

162 man herpesvirus that efficiently establishes latent infection in primary B lymphocytes.

163 ing primary infection, the virus establishes latent infection in progenitor cells of the myeloid line

164 isome maintenance and DNA replication during latent infection in proliferating cells.

165 4(+) T cells in vivo and a new mechanism for latent infection in resting CD4(+) T cells.

166 o establishes a lifetime, benign, persistent latent infection in resting memory B cells in vivo, wher

167 and HSV-2 infect many humans and establish a latent infection in sensory ganglia.

168 mplex virus 1 (HSV-1) establishes a lifelong latent infection in sensory neurons and can reactivate f

169 HSV-2 maintains a latent infection in sensory neurons and cannot be cleare

170 herpesvirus 1 (BHV-1) establishes a lifelong latent infection in sensory neurons following acute infe

171 SV) invades the nervous system and initiates latent infection in sensory neurons.

172 viruses (HSVs) is their ability to establish latent infection in sensory or autonomic ganglia and to

173 prinid herpesvirus 3 (CyHV-3), establishes a latent infection in the B cells of its host, Cyprinus ca

174 that were immunogenic during both acute and latent infection in the BAL fluid.

175 r herpesviruses, KSHV's ability to establish latent infection in the host presents a major challenge

176 Our data reveal that latent infection in the presence of DM or pre-DM, is cha

177 gest that prolonged ART may limit persistent latent infection in the T(TM) compartment.

178 nd the primary ability of HIV-1 to establish latent infection in this system to be controlled by a fo

179 ficiently infect resting CD4(+) T cells, and latent infection in those cells may arise when infected

180 owing findings: (a) R111 readily established latent infection in trigeminal ganglia; however, althoug

181 hat the viral UL144 gene is expressed during latent infection in two cell types of the myeloid lineag

182 irus exhibited impaired ability to establish latent infection in wild-type, but not STING-deficient,

183 ation-mediated transmission, reactivation of latent infections in an immunosuppressed context, or pos

184 as been the need to rely on establishment of latent infections in animal models.

185 wild-type virus results in lytic rather than latent infections in ex vivo infections of primary CD34+

186 ely due to its ability to establish lifelong latent infections in neurons and to occasionally reactiv

187 hich is characterized by its ability to form latent infections in neurons of the peripheral nervous s

188 simplex virus 1 (HSV-1) establishes lifelong latent infections in neurons within trigeminal ganglia (

189 mucocutaneous surfaces, HSVs also establish latent infections in neurons, which act as reservoirs of

190 can infect many types of cells and establish latent infections in neurons.

191 us 1 (HSV-1) establish and maintain lifelong latent infections in neurons.

192 simplex virus 1 (HSV-1) establishes lifelong latent infections in neurons.

193 tential therapeutic approaches to reactivate latent infections in quiescent cells.

194 (HIV-1) establishes transcriptionally silent latent infections in resting memory T cells and hematopo

195 e in vivo, and quiescence is correlated with latent infections in T cells.

196 buted to their ability to establish lifelong latent infections in the dorsal root ganglia (DRG).

197 roinvasive pathogens that establish lifelong latent infections in the host peripheral nervous system

198 simplex virus 1 (HSV-1) establishes lifelong latent infections in the sensory neurons of the trigemin

199 The outcomes of acute and latent infections in these different anatomic sites appe

200 chieves lifelong persistence by establishing latent infections in undifferentiated cells of the myelo

201 Herpesviruses are able to establish a latent infection, in which they escape immune detection

202 sult from acute infection or reactivation of latent infection, in which yeasts within granulomas and

203 ed cells shows the properties expected for a latent infection, including reactivation to produce newl

204 Among HIV-positive MSM, early latent infections increased from 23% to 45% (Ptrend < .0

205 ted by GATA-2 but expressed uniformly during latent infection independent of the virus isolate.

206 KSHV latent infection induces 5' untranslated region (UTR) hy

207 increased autoantibody levels for 4 to 6 wk, latent infection inhibited these responses for 1 y.

208 In persons with DM or pre-DM, latent infection is characterized by diminished circulat

209 Together, these findings suggest that a latent infection is essential for MCF induction.

210 n of viral gene expression in cells in which latent infection is established.

211 While latent infection is required for the development of KSHV

212 Epstein-Barr virus (EBV) latent infection is responsible for a variety of lymphoi

213 ty of HIV to establish a reversibly silent, "latent" infection is widely regarded as the main barrier

214 During latent infection, KSHV significantly alters mitochondria

215 tous human pathogens that establish lifelong latent infections maintained by intermittent viral react

216 up-regulate the EBNA promoter, MYC, and EBV Latent infection Membrane Proteins (LMPs), which up-regu

217 It is thought that during latent infection, Mycobacterium tuberculosis bacilli are

218 assified as having active disease (n = 3) or latent infection (n = 6), with one "percolator" monkey.

219 n this report, we show that during long-term latent infection, naive CD8 T cells are recruited into t

220 Latent infection of B lymphocytes by Epstein-Barr virus

221 nt oncogenic potential that is linked to its latent infection of B lymphocytes, during which virus re

222 disease, vaginal shedding of HSV-2 DNA, and latent infection of dorsal root ganglia in guinea pigs.

223 echanism of Nrf2 activation during prolonged latent infection of endothelial cells, using an endothel

224 The latent infection of Epstein-Barr virus (EBV) is associat

225 NF-kappaB activation is imperative for latent infection of gammaherpesviruses.

226 differentiation, aberrant accumulation, and latent infection of GC Tfh cells, resulting in marked im

227 herpesviruses, are capable of persistent and latent infection of host cells.

228 urrent study, we characterized the lytic and latent infection of HSV-1 in the CNS in comparison with

229 rough the germinal center response to ensure latent infection of long-lived memory B cells.

230 miR-92a and upregulation of CCL8 during HCMV latent infection of myeloid cells are intimately linked

231 LAcmvIL-10 is also expressed during latent infection of myeloid progenitor cells and monocyt

232 CD8(+) T cells to develop and, thus, control latent infection of neurons.

233 encoded miRNAs are expressed de novo during latent infection of primary myeloid cells.

234 analyzed the functions of LAcmvIL-10 during latent infection of primary myeloid progenitor cells and

235 -term persistence of HIV-infected cells, and latent infection of resting CD4+ T cells.

236 otactic actin activity in facilitating HIV-1 latent infection of these T cell subsets.

237 tiates early events necessary for successful latent infection of this cell type.

238 nd reactivation (LUHMES) to characterize the latent infection of two HSV-1 wild-type strains.

239 tes class I HDACs on chromatin to counteract latent infections of macrophages.

240 remains unclear whether HPV can establish a latent infection, one which may be responsible for the s

241 hether TB disease was due to reactivation of latent infection or a result of recent transmission, nor

242 Nonprimary infections due to recurrence of latent infections or reinfection with new virus strains

243 xperience primary infection, reactivation of latent infection, or reinfection with a new strain despi

244 acute infection, to efficiently establish a latent infection, or to induce VICE domain formation and

245 Latent infection persisted for several weeks and could b

246 sting that MCF might be the consequence of a latent infection rather than abortive lytic infection.

247 acterium tuberculosis infection (hereafter, "latent infection") remains poorly characterized.

248 al for EHV1 dissemination and which serve as latent infection reservoirs.

249 host immunity and may cause reactivation of latent infection, resulting in overt pulmonary, pleural,

250 ns with vaccine Oka (VOka) VZV resulted in a latent infection similar to infection with POka; however

251 culosis develop both active tuberculosis and latent infection similar to those of humans, providing a

252 hese processes often invoke lysogeny(3-6), a latent infection strategy used by temperate bacterial vi

253 nd variant H3 histones during both lytic and latent infections strengthens the hypothesis that chroma

254 nfection (such as oral hairy leukoplakia) or latent infection (such as nasopharyngeal carcinoma).

255 epithelial cells, including tumors that have latent infection, such as nasopharyngeal carcinoma (NPC)

256 ck of new lesion development in animals with latent infection suggest that innate and rapid adaptive

257 e deposited on HCMV genomes during lytic and latent infections suggesting similar mechanisms of viral

258 were substantially more permissive for HIV-1 latent infection than other CD4(+) T cells.

259 irus, Epstein-Barr virus (EBV) establishes a latent infection that can periodically undergo reactivat

260 pstein-Barr virus (EBV) establishes a stable latent infection that can persist for the life of the ho

261 a low/medium dose of C. abortus results in a latent infection that leads in a subsequent pregnancy to

262 ntegrated into the host genome, resulting in latent infections that are difficult to clear.

263 an HIV-1 cure.IMPORTANCE HIV-1 can establish latent infections that are not cleared by current antire

264 of a so-called dormant state associated with latent infections, the bacteria have to maintain basic m

265 biomarkers associated with progression from latent infection to active disease.

266 th Epstein-Barr virus follows to move from a latent infection to and through its productive cycle.

267 ts in a range of outcomes, from asymptomatic latent infections to severe systemic infection.

268 nome decline dramatically after two years of latent infection (two-sided p < 0.001, assuming an 18 h

269 tion and the proportion of individuals whose latent infection was cured after therapy.

270 molecules at significantly lower levels, but latent infection was enriched in cells expressing PD-1,

271 Latent infection was enriched in proliferating cells exp

272 criptional differences between active TB and latent infection were observed over the time course with

273 n single-copy viral load or the frequency of latent infection were observed.

274 n barrier pericytes are prone to establish a latent infection, which can be reactivated by a mixture

275 The establishment of latent infection, which is lifelong and can precede tumo

276 ggests that BHLF1 is also transcribed during latent infection, which prompted us to investigate the c

277 ved upregulation of ACVR1B expression during latent infection with a miR-UL148D deletion virus (Delta

278 g plasma cytokine levels in individuals with latent infection with DM or pre-DM (ie, intermediate hyp

279 Latent infection with Epstein-Barr virus (EBV) is respon

280 inherited chromosomally integrated HHV-6B or latent infection with HHV-6B, and (iv) HHV-6B Z29 infect

281 scent HSPCs are susceptible to predominantly latent infection with HIV-1, while actively proliferatin

282 ell-free parental Oka (POka) VZV resulted in latent infection with inability to detect several viral

283 10 European countries including testing for latent infection with M. tuberculosis by the QuantiFERON

284 sly underwent Ag-driven proliferation during latent infection with MCMV.

285 Recent latent infection with MDR M tuberculosis meant that 1.9

286 ges in the global and national prevalence of latent infection with MDR M tuberculosis.

287 to modulate T cell and cytokine responses in latent infection with Mycobacterium tuberculosis However

288 ) release assays are widely used to diagnose latent infection with Mycobacterium tuberculosis in adul

289 Latent infection with Mycobacterium tuberculosis is defi

290 al acquired immunity and is used to diagnose latent infection with Mycobacterium tuberculosis.

291 Here, we report latent infections with Bartonella quintana and a hemotro

292 After infecting the host, EBV establishes a latent infection, with low levels of messenger RNA (mRNA

293 pstein-Barr virus (EBV) maintains a lifelong latent infection within a subset of its host's memory B

294 to sensory ganglia and establish a lifelong latent infection within neurons.

295 le decrease (>0.3 log10) in the frequency of latent infection within resting CD4+ T cells.

296 urrently understood that HSV-1 establishes a latent infection within sensory peripheral neurons throu

297 BV) is a ubiquitous virus that establishes a latent infection within the host and in some cases can l

298 Our results confirm the importance of latent infection within the TCM compartment and again fo

299 n being capable of establishing long-lasting latent infections within host macrophages.

300 bout changes in the secretome that accompany latent infection, yet this is likely to be of major impo