ライフサイエンスコーパス: HIV-infected subject

1 resistance mutations at low abundance in an HIV-infected subject.

2 CCR5(+) cells, in both treated and untreated HIV-infected subjects.

3 and CD28 on HIV-specific CD4(+) T cells from HIV-infected subjects.

4 urified cell assays of samples from HCV- and HIV-infected subjects.

5 een shown to enhance T-cell function in some HIV-infected subjects.

6 but only limited study has been conducted in HIV-infected subjects.

7 ESRD in 3332 African American and 927 white HIV-infected subjects.

8 sessing properties of viruses replicating in HIV-infected subjects.

9 mRNA with either viral load or CD4 counts in HIV-infected subjects.

10 fic CD4 T cells can be detected for years in HIV-infected subjects.

11 mononuclear cells from viremic and aviremic HIV-infected subjects.

12 ted with HLH in non-renal transplant and non-HIV-infected subjects.

13 3.10-fold increased odds of neurosyphilis in HIV-infected subjects.

14 ients is similar to that seen in chronically HIV-infected subjects.

15 h potent activity against HIV-1 in vitro, in HIV-infected subjects.

16 NA loads and increased CD4+ T cell counts in HIV-infected subjects.

17 s (HIV)-uninfected subjects and 5.98-fold in HIV-infected subjects.

18 SH and csm-SH compared for 22 healthy and 36 HIV-infected subjects.

19 eron-alpha production, and clinical state of HIV-infected subjects.

20 were correlated in HIV-uninfected but not in HIV-infected subjects.

21 tment (300 microgram daily for 5 d) on eight HIV-infected subjects.

22 investigated the synthesis of LT by PMN from HIV-infected subjects.

23 poor survival in otherwise indistinguishable HIV-infected subjects.

24 antibiotic-resistant isolates than were non-HIV-infected subjects.

25 t of thymic function on the CD4/CD8 ratio of HIV-infected subjects.

26 tery was noted in 97 prospectively enrolled, HIV-infected subjects.

27 od mononuclear cells (PBMCs) of asymptomatic HIV-infected subjects.

28 tivate the CAR to ameliorate inflammation in HIV-infected subjects.

29 (IL-2) signaling in memory CD4 T cells from HIV-infected subjects.

30 nary analyses that have been unattainable in HIV-infected subjects.

31 in vascular/degenerative organ disorders in HIV-infected subjects.

32 BAL microbiome in these relatively healthy, HIV-infected subjects.

33 k of CD4(+) T-cell reconstitution in treated HIV-infected subjects.

34 tes is a potential marker of inflammation in HIV-infected subjects.

35 ombination ART (cART) on Tregs in ART-naive, HIV-infected subjects.

36 specificity of thousands of B cells from two HIV-infected subjects.

37 T cells isolated from lymph nodes of viremic HIV-infected subjects.

38 cell counts of human immunodeficiency virus (HIV)-infected subjects.

39 r prognosis in human immunodeficiency virus (HIV)-infected subjects.

40 ity of chronic human immunodeficiency virus (HIV)-infected subjects.

41 al trials with human immunodeficiency virus (HIV)-infected subjects.

42 in ART-treated human immunodeficiency virus (HIV)-infected subjects.

43 zoster (HZ) in human immunodeficiency virus (HIV)-infected subjects.

44 ing T cells in human immunodeficiency virus (HIV) -infected subjects.

45 ated from normal controls with two groups of HIV-infected subjects: (1) patients with low CD4 counts

46 ociated IFN-alpha production was observed in HIV-infected subjects (17-fold), while PDC-associated IF

47 Of 34 isolates from HIV-infected subjects, 25 were penicillin-resistant and

48 gamma 2 TCR repertoire was performed for 56 HIV-infected subjects, 51 of whom were receiving highly

49 f seronegative subjects (51%) and in 3 of 34 HIV-infected subjects (9%) (P<0.001).

50 infections in human immunodeficiency virus (HIV)-infected subjects, a randomized, double-blind, plac

51 e IgG levels after incubation in plasma from HIV-infected subjects acted as weak stimulators for HIV-

52 Polyclonal Abs isolated from HIV-infected subjects also enhanced pDC production of IF

53 s common among human immunodeficiency virus (HIV)-infected subjects, although the clinical consequenc

54 ere studied in human immunodeficiency virus (HIV)-infected subjects and uninfected control subjects.

55 e start of treatment to the CD4/CD8 ratio of HIV- infected subjects and, hence, potentially, in their

56 MRI measures, HIV serostatus, and age for 26 HIV-infected subjects and 25 seronegative subjects.

57 mortem cells and tissues obtained from three HIV-infected subjects and antemortem blood samples obtai

58 s highest in the temporal periphery for both HIV-infected subjects and control subjects.

59 ession of CD28(+) on CD8(+) cells among both HIV-infected subjects and control subjects.

60 ameters were significantly different between HIV-infected subjects and controls: increased erythrocyt

61 duction from purified CD8(+) T cells from 81 HIV-infected subjects and from 28 uninfected donors.

62 ion signatures in circulating monocytes from HIV-infected subjects and have identified a stable antia

63 Since sera from HIV-infected subjects and pooled human IgG contain antib

64 d to test for ex vivo immune responses in 85 HIV-infected subjects and showed responses to 10 of thes

65 gandan patients, including HIV-uninfected or HIV-infected subjects and those either treated with anti

66 fold were rare among this cohort of recently HIV-infected subjects and were distributed among each of

67 d hA3G (P = 0.016) mRNA levels were lower in HIV-infected subjects and were positively correlated wit

68 pression of CD163, an M2 marker, was seen in HIV-infected subjects, and CD163 inversely correlated wi

69 Thus, LT fibrosis occurs in all HIV-infected subjects, and current therapy does not reve

70 and T cells in viremic or therapy-suppressed HIV-infected subjects, and noninfected control donors.

71 accine recipients in the VAX004 trial and in HIV-infected subjects, and they point to the potential i

72 olic function was significantly decreased in HIV-infected subjects as compared to controls (mean radi

73 el and fibrosis index were both increased in HIV-infected subjects as compared to controls (P </= .04

74 tions are significantly increased in viremic HIV-infected subjects as compared with healthy subjects.

75 ing on M. tuberculosis strains isolated from HIV-infected subjects at baseline or during follow-up in

76 l tongue biopsy specimens were obtained from HIV-infected subjects before, during, and after valacycl

77 strated skewed distributions of TCR genes in HIV-infected subjects but cannot directly measure TCR di

78 une responses targeting HIV than the typical HIV-infected subject, but the exact mechanisms of how th

79 psular polysaccharides in HIV-uninfected and HIV-infected subjects by ELISA.

80 ent of humans, but isolation of hu-mAbs from HIV-infected subjects by standard methods of EBV transfo

81 progression at bay, though a small subset of HIV-infected subjects can control HIV infection without

82 In HIV-infected subjects, CCR7(-) CD8 T cells expanded at t

83 Furthermore, among HIV-infected subjects, CD4 cell counts <200 cells/mm(3)

84 In HIV-infected subjects, CD4(+) T cell surface expression

85 HAART in slowing the progression to AIDS in HIV-infected subjects, chronic immune activation and T c

86 19 +/- 23% of Harris-Benedict predictions in HIV-infected subjects compared with 102 +/- 9% for contr

87 f the left ventricle, was observed in 76% of HIV-infected subjects compared with 13% of control subje

88 ere up-regulated in multiple PBMC subsets in HIV-infected subjects compared with HIV-negative control

89 f endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons bef

90 oss 20.4% of the aortic surface volume among HIV-infected subjects, compared with 4.3% among non-HIV-

91 Sixty-two HIV-infected subjects completed the study.

92 sessed serially in 18 HIV-infected and 7 non-HIV-infected subjects consuming an ad libitum diet follo

93 We found that lymph nodes from untreated HIV-infected subjects contained an abundance of semimatu

94 amer-positive T cells in HLA-A*0201-positive HIV-infected subjects correlated with CMV-specific cytol

95 Lymph node DCs from untreated HIV-infected subjects cultured with normal allogeneic T

96 In conclusion, PMN from HIV-infected subjects demonstrate reduced 5-LO metabolis

97 The study of 25 healthy donors and 54 HIV-infected subjects demonstrated a direct correlation

98 ly higher than the incidence observed in non-HIV-infected subjects, despite the widespread use of cAR

99 Approximately 30-50% of the >30 million HIV-infected subjects develop neurological complications

100 measured in 85 human immunodeficiency virus (HIV)-infected subjects during long-term receipt of suppr

101 In multivariate analysis of the HIV-infected subjects, each 1 microg/mL above the mean o

102 of cases of IASCC was significantly lower in HIV-infected subjects engaged in an anal cytology screen

103 but not CD8(+) T cells in all categories of HIV-infected subjects evaluated, with the exception of r

104 Among HIV-infected subjects, every 100 cell/mm(3) increase in

105 s of a clinically heterogeneous sample of 62 HIV-infected subjects, examining correlations of CSF QUI

106 t-experienced, human immunodeficiency virus (HIV)-infected subjects experiencing virologic failure wh

107 While PDC from HIV-infected subjects expressed less interferon regulato

108 immediately after isolation from healthy or HIV-infected subjects failed to reveal a similar relatio

109 mpartments in relation to CD4 recovery in 21 HIV-infected subjects followed to <50 copies/ml once sta

110 on rates among human immunodeficiency virus (HIV)-infected subjects from the Adult/Adolescent Spectru

111 A cohort of 49 cART-naive HIV-infected subjects from Thailand (mean baseline CD4 c

112 1 NK cell subpopulations that differentiated HIV-infected subject groups using k-means clustering aft

113 HIV-infected subjects had a higher REE than control subj

114 Compared with the control subjects, the HIV-infected subjects had a significantly reduced IL-10

115 HIV-infected subjects had higher immune activation and m

116 rcaptoethanol-sensitive antibodies only; and HIV-infected subjects had significantly lower capsular p

117 he induction of ADCC-mediating antibodies in HIV-infected subjects has been extensively documented, t

118 PBMC from the majority of HIV-infected subjects have significant frequencies of HI

119 These findings imply that, in HIV-infected subjects, HCV may replicate in the same cel

120 Among HIV-infected subjects, highly active antiretroviral ther

121 ddressed the mechanisms of immune control in HIV-infected subjects in India, where an estimated 2.7 m

122 s of human CD4(+) and CD8(+) T cells from 57 HIV-infected subjects in varying stages of disease progr

123 gative subjects and antiretroviral-untreated HIV-infected subjects in varying stages of HIV disease w

124 NA, and 2-LTR circles in CD4(+) T cells from HIV-infected subjects infected with subtype B.

125 mplications in human immunodeficiency virus (HIV)-infected subjects initiating antiretroviral therapy

126 ption (STI) in human immunodeficiency virus (HIV)-infected subjects is currently being studied as an

127 that this down-regulation occurs in vivo in HIV-infected subjects is lacking, and viral load or vira

128 at the increased turnover of CD8+ T cells in HIV-infected subjects is mediated by the HIV envelope pr

129 aluated in 103 human immunodeficiency virus (HIV)-infected subjects (<200 CD4 cells/microL, 57; > or

130 ination of its use as an inhibitory agent in HIV-infected subjects may be informative and lead to the

131 othesized that altered platelet responses in HIV-infected subjects may contribute to altered inflamma

132 Our data indicate that viremic HIV-infected subjects may have different levels of recon

133 tum sodium intake, among chronically treated HIV-infected subjects (mean duration of ART [+/-SEM], 11

134 We studied 18 HIV-infected subjects, most with advanced immunodeficien

135 rom peripheral blood mononuclear cells of 92 HIV-infected subjects not taking antiretroviral therapy

136 data suggest that lymphocytic alveolitis in HIV-infected subjects occurs in response to viral antige

137 [+/-SEM], 11 +/- 1 years), but not among non-HIV-infected subjects of similar age and sex.

138 CHO (Efficacy Comparison in Treatment-Naive, HIV-Infected Subjects of TMC278 and Efavirenz) and THRIV

139 tive trial, 24 human immunodeficiency virus (HIV)-infected subjects on stable nucleoside or no therap

140 n this pilot double-blind study, we study 30 HIV-infected subjects on antiretroviral therapy (ART) wi

141 ly lowered markers of monocyte activation in HIV-infected subjects on antiretroviral therapy.

142 A panel from known long-term (2+ years) HIV-infected subjects on highly active antiretroviral th

143 a randomized, double-blind trial in which 20 HIV-infected subjects on stable antiretroviral regimens,

144 ctive antiretroviral therapy (HAART)-treated HIV-infected subjects or in elite controllers compared t

145 Samples were plasma obtained from HIV-infected subjects or seronegative plasma to which vi

146 duction was markedly reduced in both HCV and HIV-infected subjects (over 10-fold).

147 ected subjects, compared with 4.3% among non-HIV-infected subjects (P = .009).

148 or CMV-specific CD4(+) T cells in untreated HIV-infected subjects (p = 0.0001 and p < 0.0001, respec

149 al function in human immunodeficiency virus (HIV)-infected subjects participating in a randomized tri

150 Notably, DCs from HIV-infected subjects produced significantly higher leve

151 sessed after at least 12 weeks of therapy in HIV-infected subjects randomized to commence antiretrovi

152 Human immunodeficiency virus (HIV)-infected subjects receiving zidovudine were randomi

153 influenza A(H1N1) vaccine responsiveness in HIV-infected subjects receiving ART.

154 When administered to HIV-infected subjects receiving suppressive ART, interle

155 Since the discovery of viral reservoirs in HIV-infected subjects receiving suppressive ART, measuri

156 ater (P = 0.027, analysis of covariance) for HIV-infected subjects [REE (kJ/d) = 203.5 (kg FFM) - 123

157 In HIV-infected subjects, REE was highly correlated with fa

158 These data indicate that platelets from HIV-infected subjects release lower levels of chemokines

159 omodulation in human immunodeficiency virus (HIV)-infected subjects remain to be elucidated.

160 This study shows that PBMCs from HIV-infected subjects respond to stimulation with CpG OD

161 to antiretroviral therapy (ART)-suppressed, HIV-infected subjects resulted in plasma HIV control and

162 In HIV-infected subjects, Rev M10-transduced cells showed p

163 iciency virus-infected nonhuman primates and HIV-infected subjects revealed a correlation between YAP

164 Anergy was present in 27% of 4,058 HIV-infected subjects screened for the tuberculosis prev

165 ed individuals, as compared with symptomatic HIV-infected subjects, show limited histopathological ch

166 HIV-infected subjects showed alterations in NK activatio

167 Many of the responsive HIV-infected subjects showed recognition of multiple pep

168 therefore more similar to those observed in HIV-infected subjects, suggesting that natural hosts may

169 broad and potent neutralizing antibodies in HIV-infected subjects suggests that founder and subseque

170 In pilot studies in HIV-infected subjects, T(CM) cells appeared to have a sh

171 ntly higher in human immunodeficiency virus (HIV)-infected subjects than in uninfected subjects, and

172 L)-6, and IL-8 were significantly greater in HIV-infected subjects than control subjects after LPS ch

173 706 vs. 1346) were significantly lower among HIV-infected subjects than controls, lowest levels for t

174 (706 vs 1346) were significantly lower among HIV-infected subjects than controls, lowest levels for t

175 posterior retina was significantly lower in HIV-infected subjects than in control subjects (P < 0.00

176 energy expenditure is greater per kg FFM in HIV-infected subjects than in control subjects, which ma

177 We have identified serum antibodies from an HIV-infected subject that both were broadly neutralizing

178 In a cohort of 53 antiretroviral-naive HIV-infected subjects, the measure of thymic volume, as

179 ory symptoms and obstructive lung disease in HIV-infected subjects, the prevalence of bronchodilator

180 nonuclear cells from 6 HIV-uninfected and 25 HIV-infected subjects; the latter group included 8 long-

181 randomized 81 human immunodeficiency virus (HIV)-infected subjects to 4 interventional arms involvin

182 onducted in 36 human immunodeficiency virus (HIV)-infected subjects to evaluate its anti-HIV activity

183 ned random peptide libraries using sera from HIV-infected subjects to identify antigenic and immunoge

184 dy that acute exposure of PBMCs derived from HIV-infected subjects to IL-13 results in increased reca

185 an be applied to a variety of specimens from HIV-infected subjects to measure HIV RNA for studies of

186 anges can be used as adjuvant approaches for HIV-infected subjects, to reduce inflammation and the ri

187 nstitution" in human immunodeficiency virus (HIV)-infected subjects treated with highly active antire

188 HIV-infected subjects under virological control still ex

189 age-matched control subjects (n=39; 30.23%), HIV-infected subjects undergoing combination antiretrovi

190 osis in a contemporary group of asymptomatic HIV-infected subjects undergoing combination antiretrovi

191 Eleven HIV-infected subjects underwent repeat CSF collection si

192 ponse to six immunodominant epitopes in five HIV-infected subjects using a novel approach combining p

193 lones were isolated and characterized from 5 HIV-infected subjects, utilizing multiple HLA class I al

194 Anticryptococcal activity of PMN from HIV-infected subjects was less than that of PMN from nor

195 ly significant predictor of mortality in the HIV-infected subjects was pretransplantation MELD score

196 olating large numbers of CD4(+) T cells from HIV-infected subjects, we demonstrate that IL-7 enhances

197 d plasma viral sequence information from 765 HIV-infected subjects, we identified 64 statistically si

198 udinal, retrospective study of 117 untreated HIV-infected subjects, we show that higher frequencies a

199 Here, in a large natural history cohort of HIV-infected subjects, we show that, although leukopenia

200 -term nonprogressors (LTNPs), and vertically HIV-infected subjects were analyzed.

201 For approximately 52 mo, 1,182 HIV-infected subjects were followed.

202 and gag genes strongly suggests that all the HIV-infected subjects were infected with clade C HIV-1.

203 HIV-infected subjects were more likely to be persistent

204 alysis with BOX primers demonstrated that 12 HIV-infected subjects were persistently colonized with t

205 None of the HIV-infected subjects were receiving antiretroviral ther

206 clinical samples, samples obtained from 939 HIV-infected subjects were studied using reverse transcr

207 RCF) determinations from 752 healthy and 200 HIV-infected subjects were used to identify group-specif

208 4 weeks in 643 human immunodeficiency virus (HIV)-infected subjects who (1) had nadir CD4+ cell count

209 h levels in 30 human immunodeficiency virus (HIV)-infected subjects who had no history of cryptococco

210 roviral-naive, human immunodeficiency virus (HIV)-infected subjects who were enrolled in AIDS Clinica

211 We conducted a case-control study of HIV-infected subjects who had achieved virological suppr

212 HIV-infected subjects who had CD4 cell counts greater th

213 percentage predicted disease progression in HIV-infected subjects who initiated therapy with > 350 C

214 nguinal lymph node biopsies obtained from 10 HIV-infected subjects who received 36-52 weeks of indina

215 ong-term outcome in a cohort of asymptomatic HIV-infected subjects who underwent bronchoscopy between

216 Compared with HIV-infected subjects who were HCV seronegative, both HC

217 compared CKD incidence in a large cohort of HIV-infected subjects who were HCV seronegative, HCV vir

218 ffects of 8 weeks of sevelamer therapy on 36 HIV-infected subjects who were not receiving antiretrovi

219 ger (22-40 years) and 26 older (50-71 years) HIV-infected subjects, who were administered a comprehen

220 studied in 12 human immunodeficiency virus (HIV)-infected subjects with 50-250 CD4 T cells/mm3.

221 ) retinitis in human immunodeficiency virus (HIV)-infected subjects with or without CMV retinitis and

222 recombinant HIV envelope vaccine (rgp160) in HIV-infected subjects with > or = 400/mm3 CD4 T cells.

223 famethoxazole was significantly higher among HIV-infected subjects with <200 CD4 cells/microL than in

224 T-cell activation and DNTCs were measured in HIV-infected subjects with a nondetectable HIV load.

225 trial using a 2x2 factorial design in which HIV-infected subjects with abdominal obesity and insulin

226 beta-producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis.

227 of cytotoxic T lymphocytes from 30 untreated HIV-infected subjects with and without control of virus

228 203 (74%) of 275 subjects: 124 (80%) of 155 HIV-infected subjects with baseline isolates, 56 (69%) o

229 We randomized 45 HIV-infected subjects with CD4 counts <350 cells per mm(

230 ) when plasma Trx is chronically elevated in HIV-infected subjects with CD4 T cell counts below this

231 rotection from subsequent tuberculosis among HIV-infected subjects with childhood BCG immunization in

232 ression on blood and lymph node T cells from HIV-infected subjects with chronic disease.

233 directed toward improving mental function in HIV-infected subjects with cognitive and motor dysfuncti

234 performed a cross-sectional analysis of 223 HIV-infected subjects with data on respiratory symptoms

235 virologic parameters longitudinally among 34 HIV-infected subjects with differential outcomes.

236 Eighteen HIV-infected subjects with end-stage kidney or liver dis

237 jects with baseline isolates, 56 (69%) of 81 HIV-infected subjects with endpoint isolates, and 23 (59

238 HIV-infected subjects with HIV-1 RNA <50 copies/mL on AR

239 We compared the plasma viromes of HIV-infected subjects with low versus high CD4(+) T cell

240 pared with AM from control subjects, AM from HIV-infected subjects with normal and low CD4 counts dem

241 ipheral blood mononuclear cells (PBMCs) from HIV-infected subjects with PBMCs from uninfected donors.

242 Vaccination of HIV-infected subjects with rgp160 results in cellular an

243 lification templates, allowing genotyping in HIV-infected subjects with suppressed viral loads (e.g.,

244 that the numbers of NKT cells are reduced in HIV-infected subjects with uncontrolled viremia and mark

245 HIV-infected subjects with undetectable viral load recov

246 surface markers on peripheral NK cells from HIV-infected subjects with various degrees of HIV natura

247 and HIV-specific CD8 T cells in a cohort of HIV-infected subjects with various degrees of viral cont

248 In this large group of HIV-infected subjects with viral load suppression, ethni

249 ct in the 5-LO metabolic capacity of AM from HIV-infected subjects, with decreased expression of only

250 Although human immunodeficiency virus (HIV)-infected subjects without acquired immunodeficiency

251 Although human immunodeficiency virus (HIV)-infected subjects without AIDS have a high frequenc

252 ount were equivalent to those in 111 matched HIV-infected subjects without tuberculosis starting HAAR