ライフサイエンスコーパス: elite controller

1 ndetectable HIV RNA levels without therapy ("elite controllers").

2 ith slow disease progression (also known as "elite controllers").

3 control HIV exists, and these are known as 'elite controllers'.

4 erved in sera from long-term nonprogressors (elite controllers).

5 ntrolling chronic viral replication in these elite controllers.

6 of CD4 T cells from an unselected cohort of elite controllers.

7 individuals termed elite suppressors (ES) or elite controllers.

8 alization-resistant variants predominated in elite controllers.

9 , termed long-term nonprogressors (LTNPs) or elite controllers.

10 ne protection and viral containment in human elite controllers.

11 NAT-/serology+ blood donors, who may include elite controllers.

12 range, patients are predicted to behave like elite controllers.

13 cularly CCR5, is impaired in Nef clones from elite controllers.

14 rolled by antiviral therapy for >2 y or from elite controllers.

15 We identified 149 elite controllers (0.4%) among 34 354 persons in care.

16 7 ART-naive HIV controllers (60 of them were elite controllers), 1510 early-ART (<6 months after nega

17 .1% of hospitalizations) but were rare among elite controllers (2.7%), in whom cardiovascular hospita

18 0 ART-treated with nondetectable viremia; 30 elite controllers; 30 viremic controllers; and 30 HIV-un

19 ART-treated with non-detectable viremia; 30 elite controllers; 30 viremic controllers; and 30 HIV-un

20 mu-B*08 was significantly overrepresented in elite controllers; 38% of elite controllers were Mamu-B*

21 ivated (CD38(+)HLA-DR(+)) T cells between 30 elite controllers, 47 HIV-uninfected individuals, 187 HI

22 A total of 68 elite controllers, 68 ART recipients with suppressed vir

23 omplex (MHC) class I allele Mamu-B*08 become elite controllers after infection with simian immunodefi

24 However, elite controllers also harbor a population of HIV-specif

25 standardized uptake value, 1.53 [0.56]), the elite controller and ART-suppressed groups had intermedi

26 h-node-derived germinal center B cells of an elite controller and exhibits broad neutralization bread

27 Here, we quantify plasma HIV-1 RNA in elite controllers and correlate this with specific immun

28 4(+) T cell resistance to HIV in a cohort of elite controllers and explored transcriptional signature

29 CD4(+) T-cell counts were similar between elite controllers and HIV-negative controls but signific

30 measure of T-cell exhaustion in a cohort of elite controllers and in chronic progressors.

31 -level viremia is present in the majority of elite controllers and is associated with higher HIV-1-sp

32 natural HIV control such as that seen in HIV elite controllers and long-term nonprogressors that does

33 e a mechanism of host resistance to HIV-1 in elite controllers and may open novel perspectives for cl

34 onents of immune protection against HIV-1 in elite controllers and offer novel perspectives for the m

35 Monocytes from elite controllers (and ART recipients with suppressed vi

36 While HIV "elite controllers" and uninfected individuals had simila

37 gh and stable levels in most noncontrollers, elite controllers, and antiretroviral-treated subjects,

38 ightly differ among HIV-1 progressors, HIV-1 elite controllers, and HIV-1-negative persons.

39 V, termed long-term nonprogressors (LTNP) or elite controllers, and patients with progressive HIV inf

40 stently undetectable plasma viremia, termed "elite controllers," and a second group who achieved avir

41 Elite controllers are a distinct group, even when compar

42 Elite controllers are a heterogeneous group of people li

43 Human immunodeficiency virus type 1 (HIV-1) elite controllers are able to control virus replication

44 Elite controllers are hospitalized more frequently than

45 e is substantial evidence that at least some elite controllers are infected with replication-competen

46 nd HIV-1-negative persons, CD4+ T cells from elite controllers are less susceptible to HIV-1 infectio

47 to initiation and discontinuation of ART in elite controllers are unknown.

48 These "elite" controllers are of high interest as they may prov

49 "Elite controllers" are individuals that durably control

50 ncy virus (HIV)-infected individuals, termed elite controllers, are able to spontaneously control HIV

51 ed to HIV-associated mortality, differ among elite controllers, ART recipients with suppressed viremi

52 ssing HIV usRNA, unlike what is reported for elite controllers, but is only related to having fewer i

53 against HIV-1 infection in CD4+ T cells from elite controllers by inhibiting a cyclin-dependent kinas

54 (HAART)-treated HIV-infected subjects or in elite controllers compared to HIV-uninfected subjects.

55 factor levels were significantly elevated in elite controllers, compared with those in ART recipients

56 We performed a longitudinal study of 46 elite controllers, defined as HIV-seropositive, antiretr

57 A longitudinal analysis of 31 elite controllers demonstrated 2-5-fold fluctuations in

58 In the case of the elite controller described here, it seems likely that se

59 n 0.5% of infected individuals (here termed 'elite controllers'), despite the presence of a replicati

60 HIV-specific B cells derived from elite controllers displayed greater amounts of gp120-spe

61 Control of HIV replication in elite controller (EC) and long-term nonprogressor (LTNP)

62 An increase in potential HIV elite controllers (EC) and anecdotal reports of antiretr

63 HIV-1 elite controllers (EC) are a rare group among HIV-1-infe

64 IMPORTANCE HIV-1 elite controllers (EC) are a rare group among HIV-1-infe

65 HIV-1 elite controllers (EC) are rare individuals who are able

66 Nef clones derived from elite controllers (EC) have been shown to be attenuated

67 Human immunodeficiency virus type 1 (HIV-1) elite controllers (EC) maintain viremia below the limit

68 Elite controllers (EC) of human immunodeficiency virus t

69 Elite controllers (EC) represent a small subset of HIV-1

70 ronically infected subjects (chronic), and 7 elite controllers (EC) were used.

71 ferent virological control status, including elite controllers (EC) who maintain persistent control (

72 we attempted viral sequencing from 95 HIV-1 elite controllers (EC) who maintained plasma viral loads

73 In total, 85 samples were analyzed: 21 elite controllers (EC), 21 subjects with HIV before comb

74 Here, nef clones from 45 elite controllers (EC), 46 chronic progressors (CP), and

75 infected rhesus macaques (RM) classified as Elite Controllers (EC), and those with Low, Intermediate

76 solated from a rare subset of HIV-1-infected elite controllers (EC), with the ability to suppress vir

77 s levels (TxHIV), and therapy-naive aviremic elite controllers (EC).

78 es RNA/ml without treatment have been termed elite controllers (EC).

79 n without antiviral therapy have been termed elite controllers (EC).

80 viral load as a result of natural immunity (elite controller [EC]) or with uninfected control (HIV-)

81 levels without antiretroviral therapy (ART) (elite controllers [EC]) have the capacity to upregulate

82 s with undetectable HIV viremia without ART (elite controllers [EC]).

83 eplication without antiretroviral treatment (elite controllers [EC]).

84 Integration features of intact proviruses in elite controllers (ECs) and people on long-term therapy

85 Elite controllers (ECs) are a rare group of HIV seroposi

86 tion is reduced by as much as 10,000-fold in elite controllers (ECs) compared with typical progressor

87 These patients are called elite controllers (ECs) if they are able to maintain vir

88 Restriction of HIV-1 replication in elite controllers (ECs) is frequently attributed to T ce

89 A subset of HIV-infected individuals termed elite controllers (ECs) maintain CD4(+) T cell counts an

90 True long-term nonprogressors (LTNPs)/elite controllers (ECs) maintain durable control over HI

91 These elite controllers (ECs) mounted a broad SIV-specific CD4

92 Elite controllers (ECs) spontaneously control plasma hum

93 (HDs), 40 PHI patients, 17 Chronics, and 13 Elite controllers (ECs) were studied.

94 intact and defective proviral sequences from elite controllers (ECs), analyzing both classical escape

95 Plasma from 169 adult PWH, including 30 elite controllers (ECs), and 30 human immunodeficiency v

96 These subjects, termed elite controllers (ECs), are known to have stronger immu

97 ingly, B-cell responses were investigated in elite controllers (ECs), who maintain undetectable HIV l

98 ss than 0.5% of people living with HIV-1 are elite controllers (ECs)-individuals who maintain undetec

99 mponent in the control of HIV replication in elite controllers (ECs).

100 d in macaques that control SIVmac239, termed elite controllers (ECs).

101 eks postinfection; two of four macaques were elite controllers (ECs).

102 HIV integration increased over time in both elite controllers (ECs; n = 8) and noncontrollers (NCs;

103 suppress viremia without treatment (termed "elite controllers" [ECs]).

104 )IW9- and Vif(66-73)HW8-specific clones from elite controllers effectively suppressed SIV replication

105 on in rhesus macaques and HIV-1 infection in elite controllers, elevated levels of PD-1 expression we

106 istent viral replication occurs in untreated elite controllers even in the absence of detectable plas

107 number of HIV-infected individuals known as elite controllers experience low levels of chronic phase

108 Most of these elite controllers express the histocompatibility alleles

109 tes, we show that the proviral reservoirs of elite controllers frequently consist of oligoclonal to n

110 In addition, elite controllers had a significantly higher proportion

111 Elite controllers had favorable time to development of A

112 In conclusion, the vast majority (98%) of elite controllers had measurable plasma HIV RNA, often a

113 andable epitope-specific CD8(+) T cells from elite controllers had strong virus inhibitory capacity a

114 We found that elite controllers have a high proportion of potentially

115 contribute to this natural resistance: some elite controllers have CD4(+) T cells that produce high

116 or healthy persons not infected with HIV-1, elite controllers have circulating myeloid dendritic cel

117 ms present in this HIV-1 Envelope.IMPORTANCE Elite controllers have long provided an avenue for resea

118 ntaining undetectable plasma HIV RNA levels (elite controllers) have high HIV-specific immune respons

119 However, rare patients, termed elite controllers, have a natural ability to control HIV

120 fic T-cell responses among a large cohort of elite controllers (HIV-RNA < 75 copies/ml), "viremic" co

121 Among untreated individuals, including both elite controllers (ie, persons with a viral load of </=4

122 We examined groups of elite controllers (ie, subjects with plasma HIV RNA leve

123 The single elite controller in the cohort was an outlier on several

124 but did not significantly differ from other elite controllers in terms of HLA class I alleles, HIV-1

125 Other HLA class I alleles more common in elite controllers included HLA-B*13, HLA-B*58, and HLA-B

126 two ineffective CD8(+) T-cell clones from an elite controller into TCR-expressing lentivectors.

127 very of an immunodominant CD8-TL response in elite controller macaques against a cryptic epitope sugg

128 might play in viral control, we depleted two elite controller macaques of CD4(+) cells.

129 By contrast, virus in elite controller macaques showed little evidence of vari

130 Elite controllers maintain control of plasma HIV viremia

131 Elite controllers maintain high CD4(+) T-cell counts and

132 Elite controllers maintain undetectable levels of HIV-1

133 Human immunodeficiency virus type 1 (HIV-1) elite controllers maintain undetectable levels of viral

134 Rare individuals ('elite controllers') maintain very low levels of HIV RNA

135 It remains unclear whether elite controllers manifest T-cell exhaustion similar to

136 suggest that the T cells of these particular elite controllers may be naturally resistant to HIV infe

137 The majority of these elite controllers mount high-frequency virus-specific CD

138 Peripheral blood mononuclear cells from HIV elite controllers (n = 10), progressors (n = 12), and an

139 at the peptide level in four subject groups: elite controllers (n = 16; viral load [VL], <75 copies/m

140 ients subdivided as follows: naive (n = 63), elite controllers (n = 19), long-term nonprogressors (n

141 groups of CMV-seropositive HCT patients: (1) Elite Controllers (n = 19): did not have evidence of CMV

142 ing those with levels of < 50 RNA copies/mL (elite controllers, n = 64), those with levels of 50-2000

143 The inability of elite controller Nef to fully remove CD4 from the surfac

144 pared with HIV-1-infected subjects including elite controllers, noncontrollers, and patients receivin

145 We present observations from a HIV-1 elite controller, not treated with combination antiretro

146 escribe an unusual viral feature found in an elite controller of HIV-1 infection and demonstrate its

147 nlike most chronically infected individuals, elite controllers of HIV retain CD8(+) T-cell polyfuncti

148 nts without antiretroviral therapy (known as elite controllers or elite suppressors [ES]) is unknown.

149 natural control of HIV-1 infection known as elite controllers or suppressors (2) 72 samples from 18

150 Elite controllers or suppressors (ES) are a group of HIV

151 Elite controllers or suppressors (ES) are HIV-1-infected

152 Elite controllers or suppressors (ES) are HIV-1-infected

153 Elite controllers or suppressors (ES) are human immunode

154 A subset of HIV-1-infected patients known as elite controllers or suppressors (ES) control the virus

155 Elite controllers or suppressors (ESs) are HIV-1-infecte

156 ppressive antiretroviral therapy (ART) and 6 elite controllers or suppressors who were maintaining un

157 suppressive capacity of NK cells from HD and elite controllers or suppressors.

158 s not observed in subjects with spontaneous (elite controllers) or therapy-induced control of viral r

159 AIDS, whereas untreated animals exhibited an elite controller phenotype.

160 We demonstrate that a subgroup of elite controllers possess CD4(+) T cells that are specif

161 that is upregulated in CD4(+) T cells from "elite controllers," potently inhibited CDK2-dependent ph

162 H)1, T(H)17 and T(H)22 cells compared to the elite controller profile.

163 t were differentially regulated in resistant elite controllers relative to healthy controls.

164 he characteristics of proviral reservoirs in elite controllers remain to be determined.

165 Elite controllers represent a distinct group of individu

166 HIV elite controllers represent a remarkable minority of pat

167 Elite controllers represent a unique group of HIV-1-infe

168 imental blockade of p21 in CD4+ T cells from elite controllers resulted in a marked increase of viral

169 people spontaneously controlling the virus (elite controllers) robustly expressed genes associated w

170 After peptide stimulation, elite controllers showed a greater number of previously

171 Furthermore, CXCR5(+) CD4(+) T cells from elite controllers showed a stronger ex vivo capacity to

172 Yet, a smaller proportion of elite controllers showed an alternative gene expression

173 tion sites of intact proviral sequences from elite controllers showed an increased distance to transc

174 patients showing elevated SLAMF7 levels, and elite controllers showing levels comparable to healthy c

175 Elite controllers spontaneously suppress human immunodef

176 following primary infection and enriched in elite controllers, suggesting a critical role for these

177 Elite controllers suppress human immunodeficiency virus

178 Viremic controllers and elite controllers/suppressors maintain control over HIV-

179 l inhibitory activity of CD8(+) T cells from elite controllers than from HIV-1 progressors supports t

180 study reports the development of bnAbs in an elite controller that, along with the help of T cells, w

181 l capacity of HIV-specific CD8(+) T cells in elite controllers to inhibit HIV infection.IMPORTANCE Th

182 pared hospitalization rates and causes among elite controllers to those of immunologically intact per

183 esponses in blood and rectal mucosa from 17 "elite controllers" (viral load < 75 copies/mL), 11 "vire

184 In elite controllers, virus was detected primarily in foci

185 Moreover, in one elite controller, we were unable to detect intact provir

186 For three elite controllers, we observed increased production of M

187 Forty percent of the elite controllers were HLA-B*57 compared to twenty-three

188 iral therapy, intact proviral sequences from elite controllers were integrated at highly distinct sit

189 overrepresented in elite controllers; 38% of elite controllers were Mamu-B*08 positive compared to 3%

190 transcriptional profiles for the majority of elite controllers were similar to those of ART-treated p

191 we obtained a primary HIV-1 isolate from an elite controller who had been infected for 19 years, the

192 ir of infected memory T cells, as well as in elite controllers who limit viral replication without in

193 with different disease phenotypes, including elite controllers, who spontaneously control HIV-1 virem

194 , these data identify a specific subgroup of elite controllers whose immunological and gene expressio

195 ues control SIVmac239 replication and become elite controllers with chronic-phase viremia <1000 viral

196 e have resulted in the identification of HIV elite controllers with low or absent responses in which

197 Previous studies have shown that elite controllers with minimal effector T cell responses

198 These data indicate that elite controllers with minimal T cell responses harbor a

199 Elite controllers with the latter gene expression signat

200 lasma HIV-1 RNA levels were quantified in 90 elite controllers with use of a real time reverse-transc

201 HLA class I alleles are markedly enriched in elite controllers, with the highest association observed