ライフサイエンスコーパス: HTLV-I

1 HTLV I/II western blot confirmed six positives, whereas

2 HTLV-I and -II proviral load may be lower in sexually ac

3 HTLV-I and HTLV-II associations with higher platelet cou

4 HTLV-I core (Gag protein) complexes and the HTLV-I genom

5 HTLV-I encodes a protein known to activate several host-

6 HTLV-I encodes a regulatory protein, Tax, which is neces

7 HTLV-I encodes an oncogenic protein, Tax, which affects

8 HTLV-I has been clinically linked to the development of

9 HTLV-I or -II proviral load was 2 log10 lower in newly i

10 HTLV-I replication was inhibited by tenofovir, abacavir,

11 HTLV-I-infected ATL patients have pronounced immunodefic

12 sion of human T cell leukemia virus- type 1 (HTLV-I) between cells and between individuals, because n

13 ection with human lymphotropic virus type 1 (HTLV-I) causing HTLV-I-associated myelopathy (HAM)/tropi

14 Human T-cell leukemia virus type 1 (HTLV-I) is associated with adult T-cell leukemia (ATL),

15 Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemi

16 human T-cell leukemia/lymphoma virus type 1 (HTLV-I).

17 rovirus, human T-cell-lymphotrophic virus-1 (HTLV-I) is the etiologic agent of adult T-cell leukemia

18 wn C1q-binding peptides, derived from HIV-1, HTLV-I, and beta-amyloid.

19 , CCR2-64I, and SDF-1-3'A genotype among 116 HTLV-I-positive and 126 HTLV-I-negative persons of Afric

20 uantitative polymerase chain reaction in 122 HTLV-I- and 319 HTLV-II-infected subjects and serial VLs

21 A genotype among 116 HTLV-I-positive and 126 HTLV-I-negative persons of African descent in Jamaica we

22 V-I and HTLV-II VLs in a large cohort of 127 HTLV-I-seropositive and 328 HTLV-II-seropositive former

23 We followed 151 HTLV-I-seropositive, 387 HTLV-II-seropositive, and 799 H

24 This includes 2 HTLV-I transmissions/219 py (IR, 0.9 transmissions/100 p

25 Thirteen (5.4%) of 241 HTLV-I-negative subjects were homozygous for CCR2-64I, v

26 xamination of HTLV-I viral markers in the 28 HTLV-I-infected children provided virologic support for

27 ozygous for CCR2-64I, versus 3 (1.0%) of 291 HTLV-I-positive subjects (P=.005).

28 ver the course of 6 visits in a subset of 30 HTLV-I- and 30 HTLV-II-infected subjects.

29 ed in cervical specimens from 43 (68%) of 63 HTLV-I-infected sex workers and in samples obtained duri

30 een shown to play a major role in activating HTLV-I transcription from chromatin templates in vitro.

31 ytotoxic T-lymphocyte (CTL) response against HTLV-I-infected cells, but ultimately fail to effectivel

32 Although HTLV-I represses PDLIM2 epigenetically and specifically

33 Although HTLV-I-transformed leukemic cells have numerous genetic

34 Among HTLV-I carriers, provirus load and antibody titer were n

35 Among HTLV-I-infected children, eczema may be a cutaneous mark

36 Recently, we have generated an HTLV-I surface glycoprotein (SU) immunoadhesin, HTSU-IgG

37 ffymetrix GeneChip analysis of activated and HTLV-I-infected cells.

38 he genetic differences between activated and HTLV-I-infected lymphocytes, we performed Affymetrix Gen

39 to adult T-cell leukemia/lymphoma (ATL) and HTLV-I associated myelopathy (HAM).

40 chronic viral infections cytomegalovirus and HTLV-I.

41 6.8 nM and 8.5 nM for HIV gene, HBV gene and HTLV-I gene, respectively.

42 romoter region (TPR) in Tax-immortalized and HTLV-I-transformed cell lines.

43 etiologic agent of adult T cell leukemia and HTLV-I-associated myelopathy/tropical spastic paraparesi

44 etiologic agent of adult T cell leukemia and HTLV-I-associated myelopathy/tropical spastic paraparesi

45 proviral DNA load, HTLV-I tax mRNA load, and HTLV-I Tax-specific CD8+ T cell frequencies.

46 es of HTLV-I proviral load, HTLV-I mRNA, and HTLV-I tax-specific CD8 T cells.

47 inding, we examined HTLV-I/II serostatus and HTLV-I proviral load in 2 groups of individuals with WB

48 gate the contemporary seroprevalence of anti-HTLV I/II antibodies among solid organ donors and determ

49 T cell lymphotropic virus type I-associated (HTLV-I-associated) myelopathy/tropical spastic parapares

50 ies indicate that the counterbalance between HTLV-I/Tax and PDLIM2 may determine the outcome of HTLV-

51 dies suggest that the counterbalance between HTLV-I/Tax and PDZ-LIM domain-containing protein PDLIM2

52 TLV-I infection do not differentiate between HTLV-I asymptomatic carriers (ACs) and ATL and HAM/TSP p

53 gnificant dose-response relationship between HTLV-I transmission via breast-feeding and mother-child

54 hat a cross-reactive immune response between HTLV-I tax and neuronal hnRNP A1 is contained within the

55 VL and bladder or kidney infections for both HTLV-I (P=.005) and HTLV-II (P=.022).

56 yeloid cell line increased the titer of both HTLV-I- and HTLV-II-pseudotyped viruses.

57 transcriptional regulation of IL-15Ralpha by HTLV-I Tax.

58 that IL-15Ralpha expression was activated by HTLV-I Tax, in part, through the action of NF-kappaB.

59 aparesis (HAM/TSP) are known to be caused by HTLV-I infection.

60 activation of host immunoregulatory genes by HTLV-I, appears important in the pathogenesis of HAM/TSP

61 Although in vitro immortalization by HTLV-I virus is very efficient, we report that Tax has p

62 T cell transformation induced by HTLV-I involves the action of the 40-kDa viral Tax trans

63 interaction between persistent infection by HTLV-I and virus-specific host immunity.

64 n lymphotropic virus type 1 (HTLV-I) causing HTLV-I-associated myelopathy (HAM)/tropical spastic para

65 wer viral expression than in CD4(+) T cells, HTLV-I-infected or -activated CD14(+) cells may be a her

66 uggest that cervicitis may increase cervical HTLV-I shedding and the sexual transmission of this viru

67 A key issue in current HTLV-I research is to better understand the dynamic inte

68 ative technology that can efficiently detect HTLV-I Ab responses, we examined Ab responses for HTLV-I

69 all cell lines examined, bound no detectable HTLV-I SU.

70 rus interaction that significantly determine HTLV-I proviral load and disease risk.

71 However, current methods used to determine HTLV-I infection do not differentiate between HTLV-I asy

72 d chronic inflammatory neurological disease (HTLV-I-associated myelopathy/tropical spastic paraparesi

73 T-cell leukemia and a neurological disease, HTLV-I-associated myelopathy/tropical spastic paraparesi

74 leukemia (ATL) and the neurological disorder HTLV-I-associated myelopathy/tropical spastic paraparesi

75 ays that are differentially regulated during HTLV-I transformation.

76 easing cell surface levels of GLUT1 enhanced HTLV-I transfer, efficient virus spread correlated large

77 To confirm this hypothesis, we evaluated HTLV-I/II serostatus and proviral load in prospectively

78 he significance of this finding, we examined HTLV-I/II serostatus and HTLV-I proviral load in 2 group

79 bsets that are shown to stimulate and expand HTLV-I Tax-specific CD8+ T cells may play an important r

80 gulated expression in at least three of five HTLV-I cell lines.

81 crease in load and deduce that, for the five HTLV-I-positive patients considered here, fratricide has

82 ) and negatively with black race (P=.03) for HTLV-I and positively with smoking (P=.08) for HTLV-II.

83 ally to cell-surface protein(s) critical for HTLV-I-mediated entry in cell lines.

84 ere enrolled and prospectively evaluated for HTLV-I infection.

85 CD4+ T lymphocytes, the primary hosts for HTLV-I, undergo a series of changes that lead to T-cell

86 Moreover, immunoreactivities for HTLV-I Ags as determined by the luciferase immunoprecipi

87 nge, 0.5-5.3 log(10) copies/10(6) PBMCs) for HTLV-I and 2.60 log(10) copies/10(6) PBMCs (range, 0.05-

88 I Ab responses, we examined Ab responses for HTLV-I in serum/plasma samples from 439 subjects in Jama

89 ls that the structural motif responsible for HTLV-I RNA dimerization forms a trinucleotide RNA loop,

90 Higher HTLV-I VL was associated with previous receipt of a bloo

91 However, HTLV-I induces persistent activation of NF-kappaB, causi

92 The human T-lymphotropic virus type I (HTLV-I) causes a chronic inflammatory disorder of the ce

93 Human T-lymphotropic virus type I (HTLV-I) causes chronic infection for which there is no c

94 Human T-cell leukemia virus type I (HTLV-I) encodes a Tax oncoprotein that has crucial roles

95 ents for human T-cell leukemia virus type I (HTLV-I) entry, including the identity of the cellular re

96 gene and human T-lymphotropic virus type I (HTLV-I) gene.

97 that human T cell lymphotropic virus type I (HTLV-I) infection of CD4(+)CD25(+) Tregs in patients wit

98 children, human T lymphotropic virus type I (HTLV-I) infection was found to be associated with signif

99 bility to human T lymphotropic virus type I (HTLV-I) infection, we examined common variants in 11 imm

100 n by the human T-cell leukemia virus type I (HTLV-I) involves deregulation of cellular transcription

101 The human T-cell leukemia virus type I (HTLV-I) is an oncogenic retrovirus that is responsible f

102 Human T lymphotropic virus type I (HTLV-I) is endemic in southern Japan and the Caribbean,

103 s human T cell leukemia virus (HTLV) type I (HTLV-I) is primarily transmitted by breast-feeding or se

104 Human T cell lymphotropic virus type I (HTLV-I) is sexually transmitted.

105 Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent for adult T-cell leukemia

106 Human T cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T cell leukemia

107 Human T cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T cell leukemia

108 Human T-cell lymphotropic virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia

109 The Human T-cell leukemia virus type I (HTLV-I) is the only known transforming human retrovirus

110 s of the human T-cell leukemia virus type I (HTLV-I) oncoprotein, Tax, on genomic amplification.

111 to study human T cell leukemia virus type I (HTLV-I) replication and its inhibition by antiviral agen

112 hich the human T-cell leukemia virus type I (HTLV-I) Tax oncoprotein deregulates cellular signaling f

113 fied human T-cell lymphotropic virus type I (HTLV-I) Tax(11-19) peptide-specific T-cell populations i

114 on of the human T lymphotropic virus type I (HTLV-I) transactivator/oncoprotein, Tax, leads to faulty

115 hild human T cell lymphotropic virus type I (HTLV-I) transmission and human leukocyte antigen (HLA) c

116 alysis of human T lymphotropic virus type I (HTLV-I) viral markers in 28 Jamaican mothers and their c

117 d by the human T-cell leukemia virus type I (HTLV-I), p100 processing is very active, resulting in hi

118 by human T-cell lymphotrophic virus type I (HTLV-I), the etiologic agent of adult T-cell leukemia (A

119 Human T lymphocyte virus type I (HTLV-I)-associated chronic inflammatory neurological dis

120 Human T-cell leukemia virus type I (HTLV-I)-associated malignancies are seen in a small perc

121 Human T-lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic parapares

122 and human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic parapares

123 Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic parapares

124 ents with human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic parapares

125 n in human T-cell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic parapares

126 n by the human T-cell leukemia virus type I (HTLV-I).

127 d by the human T cell leukemia virus type I (HTLV-I).

128 aused by human T-cell leukemia virus type I (HTLV-I).

129 ) is human T cell lymphotropic virus type I (HTLV-I).

130 irus human T-cell lymphotropic virus type-I (HTLV-I) has been previously localized to a 14-nucleotide

131 Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia

132 n of human T-cell lymphotropic virus type-I (HTLV-I) to primary T cells in vitro and in ex vivo adult

133 d by human T cell lymphotropic virus type-I (HTLV-I) without curative treatment at present.

134 Human T-cell leukemia virus type-I (HTLV-I), the etiologic agent of adult T-cell leukemia (A

135 d in human T cell lymphotropic virus type-I (HTLV-I)-associated adult T cell leukemia.

136 1 (HIV-1) and human T-lymphotrophic virus-I (HTLV-I), the nuclear factor-kappaB (NF-kappaB) transcrip

137 e of human T-cell leukemia/lymphoma virus-I (HTLV-I)-infected cells is dependent upon clonal expansio

138 Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T lympho

139 Human T lymphotropic virus types I and II (HTLV-I/II) Western blot (WB) seroindeterminate status, w

140 creased upon IL-2 withdrawal in immortalized HTLV-I cell lines.

141 iR-181a, miR-150, miR-142.3p, and miR-155 in HTLV-I-infected cells in vitro and uncultured ex vivo AT

142 explanation for the mitotic abnormalities in HTLV-I-infected cells and is likely to play an important

143 of miR-124a, is constitutively activated in HTLV-I-transformed cells and ATL cells, and activating S

144 king NF-kappaB transcriptional activation in HTLV-I-transformed cells restores p53 activity.

145 ling pathways reduced telomerase activity in HTLV-I cells.

146 and exhibits constitutive kinase activity in HTLV-I-transformed T cells.

147 transcription factor known to be elevated in HTLV-I-infected cells, activated the IL-15Ralpha promote

148 dle checkpoint, which was also functional in HTLV-I-transformed cells.

149 VL was significantly higher in HTLV-I than in HTLV-II infection and was higher in HTLV-

150 regulate expression of molecules involved in HTLV-I binding and entry was examined.

151 To study initiating events involved in HTLV-I Tax-induced T cell transformation, we generated "

152 en CD8(+) T lymphocytes is known to occur in HTLV-I and possibly HSV-1 and HIV-1 infection.

153 strate an interaction between p65 and p53 in HTLV-I-transformed cells.

154 vative NHEJ DNA repair during the S phase in HTLV-I-infected Tax-expressing cells may cooperate with

155 patients but consistently down-regulated in HTLV-I cell lines, suggesting that ATL cells and in vitr

156 bly, PDLIM2 expression was down-regulated in HTLV-I-transformed T cells, and PDLIM2 reconstitution re

157 nificant differences between Ab responses in HTLV-I-infected groups may be a useful diagnostic tool i

158 ilitate viral propagation and play a role in HTLV-I-mediated disease progression.

159 Whereas Tax plays a primary role in HTLV-I-mediated NF-kappaB activation, recent studies rev

160 se occurring during the preleukemic stage in HTLV-I-infected patients.

161 precipitation (ChIP) assays, we find that in HTLV-I-transformed cells p53 and p65 form a complex on t

162 athy, but little is known about variation in HTLV-I or -II VLs by demographic characteristics and ris

163 ples from 439 subjects in Jamaica, including HTLV-I-seronegative donors, ACs, and ATL and HAM/TSP pat

164 es produce virtually no cell-free infectious HTLV-I particles.

165 g and histone modification at the integrated HTLV-I provirus in infected T-cells (SLB-1).

166 nd correlated with HTLV-I proviral DNA load, HTLV-I tax mRNA load, and HTLV-I Tax-specific CD8+ T cel

167 adapted to studies of HTLV-I proviral load, HTLV-I mRNA, and HTLV-I tax-specific CD8 T cells.

168 e pathogenesis among 51 age- and sex-matched HTLV-I carrier pairs from Japan and Jamaica.

169 This association was independent of maternal HTLV-I proviral level, antibody titer, and household inc

170 We measured HTLV-I and HTLV-II VLs in a large cohort of 127 HTLV-I-s

171 may play an important role in Tax-mediated, HTLV-I associated cellular transformation.

172 The transforming ability of HTLV-I has been largely attributed to the viral protein

173 reby suppressing the transforming ability of HTLV-I.

174 pinal fluid is proportional to the amount of HTLV-I proviral load and the levels of HTLV-I tax mRNA e

175 The association of HTLV-I infection with the most common variant, CCR2-64I,

176 upport for the epidemiologic associations of HTLV-I with seborrheic dermatitis and severe anemia in c

177 CD8(+) T cells of HTLV-I asymptomatic carriers and healthy donors did not.

178 d DHA on cell-cycle arrest and cell death of HTLV-I-infected cells.

179 Results of examination of HTLV-I viral markers in the 28 HTLV-I-infected children

180 ed, possibly as a result of the expansion of HTLV-I-infected clones.

181 Our results show a novel function of HTLV-I oncoprotein Tax as an inducer of genomic DNA doub

182 ndeterminate status may reflect a history of HTLV-I exposure.

183 review presents an overview of the impact of HTLV-I infection in general, and Tax expression in parti

184 This leads to the inability of HTLV-I-infected CD4(+)CD25(+) Tregs to inhibit the proli

185 apan and the Caribbean, but the incidence of HTLV-I-associated diseases varies across geographic area

186 nt of HTLV-I proviral load and the levels of HTLV-I tax mRNA expression.

187 riables with sequentially measured levels of HTLV-I viral markers in children.

188 ng may be part of the oncogenic mechanism of HTLV-I.

189 Mathematical modelling of HTLV-I infection, as is often the case in biology, is se

190 d disorder characterized by large numbers of HTLV-I Tax-specific CD8+ T cells.

191 protein PDLIM2 may determine the outcome of HTLV-I infection.

192 /Tax and PDLIM2 may determine the outcome of HTLV-I infection.

193 of 85 initially seronegative sex partners of HTLV-I and -II carriers seroconverted, for an incidence

194 s may be associated with the pathogenesis of HTLV-I-associated neurologic disease.

195 lay an important role in the pathogenesis of HTLV-I-associated neurological disease.

196 perimental hypotheses for the persistence of HTLV-I in vivo have led to the development of mathematic

197 nd host immunity during the chronic phase of HTLV-I infection offers important insights regarding the

198 c activity when expressed in the presence of HTLV-I Tax, mutated p53 R276H, or c-Myc F138C found in h

199 ulatory loop leading to the proliferation of HTLV-I infected cells.

200 eacetylases participate in the regulation of HTLV-I transcription in infected T-cells.

201 re demonstrated to be the major reservoir of HTLV-I provirus as well as Tax11-19 peptide-HLA-A*201 co

202 The Ab responses of HTLV-I-infected subjects differed significantly from tho

203 and maternal cells may influence the risk of HTLV-I infection by breast-feeding, perhaps because anti

204 sequilibrium with it, may affect the risk of HTLV-I infection in a recessive manner.

205 ema may be a cutaneous marker of the risk of HTLV-I-associated diseases developing in adulthood.

206 The role of HTLV-I-specific CD8 T cell immune responses is highlight

207 ce and risk factors for cervical shedding of HTLV-I DNA among Peruvian sex workers.

208 ver, the mechanism of cell-to-cell spread of HTLV-I is not understood.

209 hniques that have been adapted to studies of HTLV-I proviral load, HTLV-I mRNA, and HTLV-I tax-specif

210 The susceptibility of HTLV-I to 6 nucleoside reverse-transcriptase inhibitors

211 mission of HTLV-II may be similar to that of HTLV-I, and female-to-male transmission may play a more

212 ch has been shown to enhance transmission of HTLV-I in vitro, is found at high levels in breast milk

213 etween HLA class I types and transmission of HTLV-I were analyzed using proportional-hazards regressi

214 ive and quantitative effect of fratricide on HTLV-I equilibrium proviral load.

215 /TSP will enhance our understanding of other HTLV-I-associated disorders plus other neurologic, hemat

216 ogical disorder tropical spastic paraparesis/HTLV-I-associated myelopathy.

217 and the frequency of potentially pathogenic HTLV-I-specific CD8(+) cells.

218 g the role of a specific viral gene product (HTLV-I Tax) on the expression of genes associated with T

219 erate with other functions of Tax to promote HTLV-I-associated adult T-cell leukemia.

220 e individuals may be infected with prototype HTLV-I.

221 66 WB seronegative patients who had received HTLV-I-infected blood products by transfusion.

222 uman leukocyte antigen type A*201-restricted HTLV-I Tax11-19 tetramer, we detected virus-specific CD8

223 rs of the CNS, including multiple sclerosis, HTLV-I associated myelopathy/tropical spastic paraparesi

224 e CD8(+) T cells were effective at targeting HTLV-I-infected cells.

225 isorder of the central nervous system termed HTLV-I-associated myelopathy/tropical spastic paraparesi

226 We further found that HTLV-I- and Tax-transformed cells are not more susceptib

227 These studies indicated that HTLV-I-transformed and ATL cells, but not normal periphe

228 We demonstrated previously that HTLV-I Tax oncoprotein is a potent inducer of p100 proce

229 Here we report that HTLV-I has also evolved a protein that interferes with T

230 Here we show that HTLV-I-transformed T cells progress through S/G(2)/M pha

231 These data suggest that HTLV-I Tax alters the genomic stability of cells, an eff

232 Our results suggest that HTLV-I-infected cells have an unbalanced expression of m

233 Collectively, the results suggest that HTLV-I/II WB seroindeterminate status may reflect a hist

234 The HTLV-I antibody titer increased significantly up to 1 ye

235 The HTLV-I antibody titer was determined using the Vironstik

236 The HTLV-I protein Tax alters gene expression, including tho

237 The HTLV-I protein Tax is well known as a transcriptional tr

238 The HTLV-I proviral DNA load remained unchanged.

239 The HTLV-I provirus DNA load was measured using the Taqman s

240 The HTLV-I Tax protein is essential for clinical manifestati

241 The HTLV-I Tax-specific antibody titers were measured using

242 The HTLV-I transactivator protein Tax plays an integral role

243 The HTLV-I transforming protein Tax functions as an intracel

244 The HTLV-I-encoded protein tax constitutively activates inte

245 erplay that occurs between NF-kappaB and the HTLV-I and HIV-1 retroviral pathogens.

246 HTLV-I core (Gag protein) complexes and the HTLV-I genome accumulate at the cell-cell junction and a

247 MBP-ghC showed a preference for IgM and the HTLV-I gp21 peptide.

248 proinflammatory cytokines, microbes, and the HTLV-I Tax oncoprotein.

249 on, infected target cell activation, and the HTLV-I-specific CTL response.

250 he cellular regulatory proteins bound at the HTLV-I promoter in vivo is not known.

251 nd both p300 and CREB-binding protein at the HTLV-I promoter.

252 vitro activation and suggest a role for the HTLV-I SU binding proteins in the immunobiology of CD4(+

253 and defined a new CD8+ T-cell epitope in the HTLV-I envelope region.

254 eneration of the first structural map of the HTLV-I DIS.

255 Previous studies using a soluble form of the HTLV-I envelope protein SU have shown that quiescent hum

256 Here, expression of the HTLV-I SU binding protein on primary cells of the immune

257 D4(+)CD25(-) Tregs, due to the effect of the HTLV-I tax gene.

258 an increase in histone H4 acetylation on the HTLV-I promoter and a concomitant increase in viral RNA.

259 Interferon-beta1a therapy reduced the HTLV-I tax messenger RNA load and the frequency of poten

260 Tax both stimulates the HTLV-I long terminal repeat and deregulates the expressi

261 It is possible that the HTLV-I Tax-mediated induction of IL-15Ralpha and IL-15 m

262 We have also shown that the HTLV-I-encoded Tax protein is able to activate Tpl2/Cot

263 expression of human PTTG cooperated with the HTLV-I Tax oncoprotein in cellular transformation.

264 xpression that inversely correlated with the HTLV-I tax proviral load, loss of Treg suppressor functi

265 of TGF-betaRII inversely correlated with the HTLV-I tax proviral load.

266 Antibodies to HTLV-I/II, HIV-1, EBV, and CMV were measured using stand

267 In 1989, children born to HTLV-I-infected mothers in Jamaica were enrolled and pro

268 elated genes among Jamaican children born to HTLV-I-seropositive mothers.

269 In contrast to HTLV-I virions, the soluble HTSU-IgG did not effect T-ce

270 own about the innate immunity of the host to HTLV-I infection.

271 /TSP) is associated with immunoreactivity to HTLV-I tax.

272 NF-kappaB activation was closely linked to HTLV-I viral protein expression.

273 HAM/TSP and monoclonal antibodies (MAbs) to HTLV-I tax stained neurons.

274 cell fratricide with particular reference to HTLV-I infection.

275 e the differences in host immune response to HTLV-I infection in 2 populations.

276 IL-15Ralpha promoter that were responsive to HTLV-I Tax.

277 tory genes could influence susceptibility to HTLV-I infection.

278 The virus-encoded transactivating HTLV-I tax gene was demonstrated to have a direct inhibi

279 n interleukin (IL)-2-independent transformed HTLV-I cells, Tax strongly activates the hTERT promoter

280 After cell-to-cell transmission, HTLV-I increases its viral genome by de novo infection a

281 These results were confirmed using HTLV-I molecular clones expressing Tax at physiological

282 dy titer was determined using the Vironstika HTLV-I/II Microelisa System (Organon Teknika).

283 Type I human T cell leukemia virus (HTLV-I) is etiologically linked with adult T cell leukem

284 s to ask if the human T-cell leukemia virus (HTLV-I) Tax protein, which also interacts with CR2, comp

285 The human T-cell leukemia virus (HTLV-I)-encoded Tax protein is a potent transcriptional

286 between ex vivo ATL tumor cells and in vitro HTLV-I cell lines.

287 A cohort of 85 HTLV-positive (30 with HTLV-I and 55 with HTLV-II) blood donors and their stabl

288 r cancers and other diseases associated with HTLV-I infection and/or PDLIM2 deregulation.

289 C/-1116G) were significantly associated with HTLV-I infection in children independent of maternal pro

290 in neurodegenerative disease associated with HTLV-I infection.

291 -3.7) were not significantly associated with HTLV-I shedding.

292 Compared with HTLV-I seronegatives, haplotypes of IL6 (-660G/-635C/-23

293 be increased in HAM/TSP and correlated with HTLV-I proviral DNA load, HTLV-I tax mRNA load, and HTLV

294 ory joint diseases in patients infected with HTLV-I by repressing transcription of the TNF-alpha gene

295 Participants with HTLV-I and HTLV-II had higher adjusted platelet counts (

296 to that of cells isolated from patients with HTLV-I-associated adult T-cell leukemia or with progeria

297 550 in the treatment of select patients with HTLV-I-associated ATL and HAM/TSP.

298 tion of CD4(+)CD25(+) Tregs in patients with HTLV-I-associated myelopathy/tropical spastic paraparesi

299 mononuclear cells (PBMCs) from patients with HTLV-I-associated neurologic disease and defined a new C

300 Over the course of a median of 10.4 years, HTLV-I VLs decreased slightly (slope, -0.017 log(10) cop