ライフサイエンスコーパス: latent infection

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

2 viral cyclin that promotes reactivation from latent infection.

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

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

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

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

7 episomes inside the host cell nucleus during latent infection.

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

9 rant lytic gene expression and impaired KSHV latent infection.

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

11 arbor this virus allowing the persistence of latent infection.

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

13 ral gene expression and the establishment of latent infection.

14 IKKbeta and IKKepsilon that were crucial for latent infection.

15 ased KSHV lytic gene expression and impaired latent infection.

16 s share a remarkable propensity to establish latent infection.

17 HV has evolved with strategies to facilitate latent infection.

18 tion of infectious agents or reactivation of latent infection.

19 ymphocyte pool through a growth-transforming latent infection.

20 reduced gene expression under conditions of latent infection.

21 HIV infection, including both productive and latent infection.

22 on than disease resulting from activation of latent infection.

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

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

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

26 th positive skin tests risks underestimating latent infection.

27 ese treatments in preventing reactivation of latent infection.

28 BCG efficacy but not prevent reactivation of latent infection.

29 tion of immediate-early (IE) genes following latent infection.

30 outcomes ranging from bacterial clearance to latent infection.

31 M. tuberculosis and prevents reactivation of latent infection.

32 uman pathogens that switch between lytic and latent infection.

33 -Jkappa cognate site in establishing primary latent infection.

34 ar proteins during its replicative cycle and latent infection.

35 vels also remained reduced during persistent/latent infection.

36 lthough most affected individuals maintain a latent infection.

37 nates are breastfed by mothers with acute or latent infection.

38 latency, none has demonstrated clearance of latent infection.

39 iP) is required for episome stability during latent infection.

40 ange of both viral and cellular genes during latent infection.

41 ar agents, particularly for the treatment of latent infection.

42 s can result in active TB or, more commonly, latent infection.

43 jacks the repressor to silence itself during latent infection.

44 rvous system and persist there as a lifelong latent infection.

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

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

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

48 RNA species may contribute significantly to latent infection.

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

50 LANA) E3 ligase activity in gammaherpesvirus latent infection.

51 o the development of strategies to eliminate latent infection.

52 differentially expressed mRNAs in active and latent infection.

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

54 iscriminated between active tuberculosis and latent infection.

55 e septicemia to chronic localized illness or latent infection.

56 e various cellular pathways to establish the latent infection.

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

58 s characteristic of reactivation of lifelong latent infections.

59 ding the host immune system and establishing latent infections.

60 are human pathogens that establish lytic and latent infections.

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

62 B lymphocyte signaling to achieve persistent latent infections.

63 , maintain, and reactivate HCMV experimental latent infections.

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

65 adaptive TGF-beta signaling during acute and latent infections.

66 n of transgenic CD4 T cells during acute and latent infections.

67 ipts that are produced during productive and latent infections.

68 d diseases but also in other viruses causing latent infections.

69 licating bacteria associated with chronic or latent infections.

70 iruses that establish acute, persistent, and latent infections.

71 at determines the outcomes of both lytic and latent infections.

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

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

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

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

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

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

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

79 During latent infection, a restricted gene expression program l

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

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

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

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

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

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

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

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

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

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

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

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

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

93 that a restrictive histone code could govern latent infection and that either dissipation of the hist

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

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

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

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

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

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

100 Both latent infection and viral protein expression contribute

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

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

103 ) T cells can influence the outcome of HSV-1 latent infection, and manipulating Gal-9 signals might r

104 fectors for the control of gamma-herpesvirus latent infection, and they mediate this effect by two in

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

106 Latent infection appears to wane within the transitional

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

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

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

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

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

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

113 The degree of latent infection by an EBV mutant defective in the prima

114 Latent infection by Kaposi's sarcoma-associated herpesvi

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

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

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

118 ings illuminate the mechanisms through which latent infection can be established in HPCs and suggest

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

120 To determine if KHV latent infections can be reactivated, six koi were subje

121 ma-associated herpesvirus establish lifelong latent infections, can reactivate in immunocompromised i

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

123 HSV establishes latent infections characterized by suppression of viral

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

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

126 proteins remained unchanged, suggesting that latent infection disrupted endothelial cell junctions.

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

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

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

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

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

132 e of the unique features of Herpesviridae is latent infection following a primary infection.

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

134 ulation in mice, cannot establish detectable latent infection following different routes of infection

135 t virus replication and the establishment of latent infection following intranasal inoculation.

136 injection and cannot establish a detectable latent infection following subcutaneous (s.c.) immunizat

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

138 ile 8 and 4 samples showed expression of the latent infection genes encoding isocitrate lyase and alp

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

140 Viral latent infections have numerous associated pathologies,

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

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

143 Preventing active TB and tackling latent infection in addition to the Directly Observed Tr

144 2 decades of life and establishes reversible latent infection in B cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 RHVP establishes acute and latent infection in laboratory mice.

160 s was previously shown to be associated with latent infection in mice and may also play a role in rea

161 ly reduces the ability of MHV68 to establish latent infection in mice, consistent with the possibilit

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

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

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

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

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

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

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

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

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

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

172 4(+) T cells in vivo and a new mechanism for latent infection in resting CD4(+) T cells.

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

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

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

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

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

178 plex virus 1 (HSV-1) can establish life-long latent infection in sensory neurons, from which periodic

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

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

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

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

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

184 functions, thereby aiding the maintenance of latent infection in the face of the host immune response

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

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

187 We further show that the establishment of latent infection in these cells can be reversed by tumor

188 ent spontaneous lytic activation and promote latent infection in this compartment.

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

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

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

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

193 cytomegalovirus (HCMV) that is required for latent infection in vitro.

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

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

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

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

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

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

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

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

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

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

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

205 ntry into the body, the virus establishes a "latent" infection in which viral DNA is silenced with th

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

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

208 Infected BJAB cells display signatures of latent infection, including classical latency-associated

209 st immune response were downregulated during latent infection, including genes for CD80, CD86, and th

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

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

212 In conclusion, KSHV latent infection increases Rac1 and PAK1 activity in end

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

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

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

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

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

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

219 While latent infection is required for the development of KSHV

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

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

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

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

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

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

226 that oral transmission of KSHV involves the latent infection of a subset of tonsillar IgMl-expressin

227 Latent infection of B lymphocytes by Epstein-Barr virus

228 tained as an extrachromosomal episome during latent infection of B lymphocytes.

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

230 Latent infection of EBV is linked to the development of

231 During latent infection of endothelial cells, KSHV induces aero

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

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

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

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

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

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

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

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

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

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

242 c acid, that activates LIMK and promotes HIV latent infection of resting CD4 T cells.

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

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

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

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

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

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

249 ulosis infection in humans results in either latent infection or active tuberculosis.

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

251 Latent infection persisted for several weeks and could b

252 The ability of HIV-1 to establish a latent infection presents a barrier to curing HIV.

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

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

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

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

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

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

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

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

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

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

263 Thus, for this latent infection, T cells subjected to chronic Ag stimul

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

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

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

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

268 Monkeys with latent infection that were randomized to receive TNF-neu

269 During latent infection, the majority of Kaposi's sarcoma-assoc

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

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

272 ired cohorts of individuals with and without latent infection (total N = 19 886).

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

274 n of breast milk collected from mothers with latent infection was sufficient to transfer MCMV to neon

275 ssed by HSV-1 or HSV-2 during productive and latent infection, we applied a massively parallel sequen

276 Control monkeys with latent infection were given no treatment or saline.

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

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

279 ed with Mycobacterium tuberculosis develop a latent infection, which does not progress to active tube

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

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

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

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

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

285 10 European countries including testing for latent infection with M. tuberculosis by the QuantiFERON

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

287 Latent infection with Mycobacterium tuberculosis is defi

288 One-third of the world's population has latent infection with Mycobacterium tuberculosis, and 10

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

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

291 tomegalovirus (HCMV) persists as a life-long latent infection, with host immunosuppression often resu

292 s a herpesvirus that establishes a lifelong, latent infection within a host.

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