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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  of CD4 T cells from an unselected cohort of elite controllers.
6 individuals termed elite suppressors (ES) or elite controllers.
7 alization-resistant variants predominated in elite controllers.
8 , termed long-term nonprogressors (LTNPs) or elite controllers.
9 ne protection and viral containment in human elite controllers.
10 range, patients are predicted to behave like elite controllers.
11 cularly CCR5, is impaired in Nef clones from elite controllers.
12 rolled by antiviral therapy for >2 y or from elite controllers.
13 ntrolling chronic viral replication in these elite controllers.
14                            We identified 149 elite controllers (0.4%) among 34 354 persons in care.
15 .1% of hospitalizations) but were rare among elite controllers (2.7%), in whom cardiovascular hospita
16 mu-B*08 was significantly overrepresented in elite controllers; 38% of elite controllers were Mamu-B*
17 ivated (CD38(+)HLA-DR(+)) T cells between 30 elite controllers, 47 HIV-uninfected individuals, 187 HI
18                                A total of 68 elite controllers, 68 ART recipients with suppressed vir
19 omplex (MHC) class I allele Mamu-B*08 become elite controllers after infection with simian immunodefi
20                                     However, elite controllers also harbor a population of HIV-specif
21 standardized uptake value, 1.53 [0.56]), the elite controller and ART-suppressed groups had intermedi
22        Here, we quantify plasma HIV-1 RNA in elite controllers and correlate this with specific immun
23 4(+) T cell resistance to HIV in a cohort of elite controllers and explored transcriptional signature
24    CD4(+) T-cell counts were similar between elite controllers and HIV-negative controls but signific
25  measure of T-cell exhaustion in a cohort of elite controllers and in chronic progressors.
26 -level viremia is present in the majority of elite controllers and is associated with higher HIV-1-sp
27 e a mechanism of host resistance to HIV-1 in elite controllers and may open novel perspectives for cl
28 onents of immune protection against HIV-1 in elite controllers and offer novel perspectives for the m
29                               Monocytes from elite controllers (and ART recipients with suppressed vi
30                                   While HIV "elite controllers" and uninfected individuals had simila
31 gh and stable levels in most noncontrollers, elite controllers, and antiretroviral-treated subjects,
32 ightly differ among HIV-1 progressors, HIV-1 elite controllers, and HIV-1-negative persons.
33 V, termed long-term nonprogressors (LTNP) or elite controllers, and patients with progressive HIV inf
34                                              Elite controllers are a distinct group, even when compar
35  Human immunodeficiency virus type 1 (HIV-1) elite controllers are able to control virus replication
36                                              Elite controllers are hospitalized more frequently than
37 nd HIV-1-negative persons, CD4+ T cells from elite controllers are less susceptible to HIV-1 infectio
38  to initiation and discontinuation of ART in elite controllers are unknown.
39                                       These "elite" controllers are of high interest as they may prov
40                                             "Elite controllers" are individuals that durably control
41 ncy virus (HIV)-infected individuals, termed elite controllers, are able to spontaneously control HIV
42 ed to HIV-associated mortality, differ among elite controllers, ART recipients with suppressed viremi
43 against HIV-1 infection in CD4+ T cells from elite controllers by inhibiting a cyclin-dependent kinas
44  (HAART)-treated HIV-infected subjects or in elite controllers compared to HIV-uninfected subjects.
45 factor levels were significantly elevated in elite controllers, compared with those in ART recipients
46      We performed a longitudinal study of 46 elite controllers, defined as HIV-seropositive, antiretr
47                A longitudinal analysis of 31 elite controllers demonstrated 2-5-fold fluctuations in
48            HIV-specific B cells derived from elite controllers displayed greater amounts of gp120-spe
49                Control of HIV replication in elite controller (EC) and long-term nonprogressor (LTNP)
50                                        HIV-1 elite controllers (EC) are rare individuals who are able
51                      Nef clones derived from elite controllers (EC) have been shown to be attenuated
52  Human immunodeficiency virus type 1 (HIV-1) elite controllers (EC) maintain viremia below the limit
53                                              Elite controllers (EC) of human immunodeficiency virus t
54 ronically infected subjects (chronic), and 7 elite controllers (EC) were used.
55  we attempted viral sequencing from 95 HIV-1 elite controllers (EC) who maintained plasma viral loads
56                     Here, nef clones from 45 elite controllers (EC), 46 chronic progressors (CP), and
57  infected rhesus macaques (RM) classified as Elite Controllers (EC), and those with Low, Intermediate
58 solated from a rare subset of HIV-1-infected elite controllers (EC), with the ability to suppress vir
59 s levels (TxHIV), and therapy-naive aviremic elite controllers (EC).
60 es RNA/ml without treatment have been termed elite controllers (EC).
61 n without antiviral therapy have been termed elite controllers (EC).
62  viral load as a result of natural immunity (elite controller [EC]) or with uninfected control (HIV-)
63 levels without antiretroviral therapy (ART) (elite controllers [EC]) have the capacity to upregulate
64 eplication without antiretroviral treatment (elite controllers [EC]).
65                                              Elite controllers (ECs) are a rare group of HIV seroposi
66 tion is reduced by as much as 10,000-fold in elite controllers (ECs) compared with typical progressor
67  A subset of HIV-infected individuals termed elite controllers (ECs) maintain CD4(+) T cell counts an
68        True long-term nonprogressors (LTNPs)/elite controllers (ECs) maintain durable control over HI
69                                        These elite controllers (ECs) mounted a broad SIV-specific CD4
70  (HDs), 40 PHI patients, 17 Chronics, and 13 Elite controllers (ECs) were studied.
71                       These subjects, termed elite controllers (ECs), are known to have stronger immu
72 ingly, B-cell responses were investigated in elite controllers (ECs), who maintain undetectable HIV l
73 d in macaques that control SIVmac239, termed elite controllers (ECs).
74 eks postinfection; two of four macaques were elite controllers (ECs).
75 mponent in the control of HIV replication in elite controllers (ECs).
76  HIV integration increased over time in both elite controllers (ECs; n = 8) and noncontrollers (NCs;
77  suppress viremia without treatment (termed "elite controllers" [ECs]).
78 )IW9- and Vif(66-73)HW8-specific clones from elite controllers effectively suppressed SIV replication
79 on in rhesus macaques and HIV-1 infection in elite controllers, elevated levels of PD-1 expression we
80 istent viral replication occurs in untreated elite controllers even in the absence of detectable plas
81  number of HIV-infected individuals known as elite controllers experience low levels of chronic phase
82                                Most of these elite controllers express the histocompatibility alleles
83                                 In addition, elite controllers had a significantly higher proportion
84                                              Elite controllers had favorable time to development of A
85    In conclusion, the vast majority (98%) of elite controllers had measurable plasma HIV RNA, often a
86 andable epitope-specific CD8(+) T cells from elite controllers had strong virus inhibitory capacity a
87                                We found that elite controllers have a high proportion of potentially
88  contribute to this natural resistance: some elite controllers have CD4(+) T cells that produce high
89  or healthy persons not infected with HIV-1, elite controllers have circulating myeloid dendritic cel
90 ntaining undetectable plasma HIV RNA levels (elite controllers) have high HIV-specific immune respons
91               However, rare patients, termed elite controllers, have a natural ability to control HIV
92 fic T-cell responses among a large cohort of elite controllers (HIV-RNA < 75 copies/ml), "viremic" co
93  Among untreated individuals, including both elite controllers (ie, persons with a viral load of </=4
94                        We examined groups of elite controllers (ie, subjects with plasma HIV RNA leve
95                                   The single elite controller in the cohort was an outlier on several
96  but did not significantly differ from other elite controllers in terms of HLA class I alleles, HIV-1
97     Other HLA class I alleles more common in elite controllers included HLA-B*13, HLA-B*58, and HLA-B
98 two ineffective CD8(+) T-cell clones from an elite controller into TCR-expressing lentivectors.
99 very of an immunodominant CD8-TL response in elite controller macaques against a cryptic epitope sugg
100 might play in viral control, we depleted two elite controller macaques of CD4(+) cells.
101                        By contrast, virus in elite controller macaques showed little evidence of vari
102                                              Elite controllers maintain control of plasma HIV viremia
103                                              Elite controllers maintain high CD4(+) T-cell counts and
104                                              Elite controllers maintain undetectable levels of HIV-1
105  Human immunodeficiency virus type 1 (HIV-1) elite controllers maintain undetectable levels of viral
106                           Rare individuals ('elite controllers') maintain very low levels of HIV RNA
107                   It remains unclear whether elite controllers manifest T-cell exhaustion similar to
108 suggest that the T cells of these particular elite controllers may be naturally resistant to HIV infe
109                        The majority of these elite controllers mount high-frequency virus-specific CD
110  Peripheral blood mononuclear cells from HIV elite controllers (n = 10), progressors (n = 12), and an
111 at the peptide level in four subject groups: elite controllers (n = 16; viral load [VL], <75 copies/m
112 ients subdivided as follows: naive (n = 63), elite controllers (n = 19), long-term nonprogressors (n
113 ing those with levels of < 50 RNA copies/mL (elite controllers, n = 64), those with levels of 50-2000
114                             The inability of elite controller Nef to fully remove CD4 from the surfac
115 pared with HIV-1-infected subjects including elite controllers, noncontrollers, and patients receivin
116         We present observations from a HIV-1 elite controller, not treated with combination antiretro
117 nlike most chronically infected individuals, elite controllers of HIV retain CD8(+) T-cell polyfuncti
118 nts without antiretroviral therapy (known as elite controllers or elite suppressors [ES]) is unknown.
119  natural control of HIV-1 infection known as elite controllers or suppressors (2) 72 samples from 18
120                                              Elite controllers or suppressors (ES) are a group of HIV
121                                              Elite controllers or suppressors (ES) are HIV-1-infected
122                                              Elite controllers or suppressors (ES) are HIV-1-infected
123                                              Elite controllers or suppressors (ES) are human immunode
124 A subset of HIV-1-infected patients known as elite controllers or suppressors (ES) control the virus
125                                              Elite controllers or suppressors (ESs) are HIV-1-infecte
126 ppressive antiretroviral therapy (ART) and 6 elite controllers or suppressors who were maintaining un
127 s not observed in subjects with spontaneous (elite controllers) or therapy-induced control of viral r
128 AIDS, whereas untreated animals exhibited an elite controller phenotype.
129            We demonstrate that a subgroup of elite controllers possess CD4(+) T cells that are specif
130  that is upregulated in CD4(+) T cells from "elite controllers," potently inhibited CDK2-dependent ph
131 t were differentially regulated in resistant elite controllers relative to healthy controls.
132                                              Elite controllers represent a distinct group of individu
133                                              Elite controllers represent a unique group of HIV-1-infe
134 imental blockade of p21 in CD4+ T cells from elite controllers resulted in a marked increase of viral
135                   After peptide stimulation, elite controllers showed a greater number of previously
136    Furthermore, CXCR5(+) CD4(+) T cells from elite controllers showed a stronger ex vivo capacity to
137                 Yet, a smaller proportion of elite controllers showed an alternative gene expression
138                                              Elite controllers spontaneously suppress human immunodef
139  following primary infection and enriched in elite controllers, suggesting a critical role for these
140                                              Elite controllers suppress human immunodeficiency virus
141                      Viremic controllers and elite controllers/suppressors maintain control over HIV-
142 l inhibitory activity of CD8(+) T cells from elite controllers than from HIV-1 progressors supports t
143 study reports the development of bnAbs in an elite controller that, along with the help of T cells, w
144 l capacity of HIV-specific CD8(+) T cells in elite controllers to inhibit HIV infection.IMPORTANCE Th
145 pared hospitalization rates and causes among elite controllers to those of immunologically intact per
146 esponses in blood and rectal mucosa from 17 "elite controllers" (viral load < 75 copies/mL), 11 "vire
147                                           In elite controllers, virus was detected primarily in foci
148                                    For three elite controllers, we observed increased production of M
149                         Forty percent of the elite controllers were HLA-B*57 compared to twenty-three
150 overrepresented in elite controllers; 38% of elite controllers were Mamu-B*08 positive compared to 3%
151 transcriptional profiles for the majority of elite controllers were similar to those of ART-treated p
152 with different disease phenotypes, including elite controllers, who spontaneously control HIV-1 virem
153 , these data identify a specific subgroup of elite controllers whose immunological and gene expressio
154 ues control SIVmac239 replication and become elite controllers with chronic-phase viremia <1000 viral
155 e have resulted in the identification of HIV elite controllers with low or absent responses in which
156             Previous studies have shown that elite controllers with minimal effector T cell responses
157                     These data indicate that elite controllers with minimal T cell responses harbor a
158                                              Elite controllers with the latter gene expression signat
159 lasma HIV-1 RNA levels were quantified in 90 elite controllers with use of a real time reverse-transc
160 HLA class I alleles are markedly enriched in elite controllers, with the highest association observed

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