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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.
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
19 omplex (MHC) class I allele Mamu-B*08 become elite controllers after infection with simian immunodefi
21 standardized uptake value, 1.53 [0.56]), the elite controller and ART-suppressed groups had intermedi
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
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
31 gh and stable levels in most noncontrollers, elite controllers, and antiretroviral-treated subjects,
33 V, termed long-term nonprogressors (LTNP) or elite controllers, and patients with progressive HIV inf
35 Human immunodeficiency virus type 1 (HIV-1) elite controllers are able to control virus replication
37 nd HIV-1-negative persons, CD4+ T cells from elite controllers are less susceptible to HIV-1 infectio
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
52 Human immunodeficiency virus type 1 (HIV-1) elite controllers (EC) maintain viremia below the limit
55 we attempted viral sequencing from 95 HIV-1 elite controllers (EC) who maintained plasma viral loads
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
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
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
72 ingly, B-cell responses were investigated in elite controllers (ECs), who maintain undetectable HIV l
76 HIV integration increased over time in both elite controllers (ECs; n = 8) and noncontrollers (NCs;
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
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
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
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
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
99 very of an immunodominant CD8-TL response in elite controller macaques against a cryptic epitope sugg
105 Human immunodeficiency virus type 1 (HIV-1) elite controllers maintain undetectable levels of viral
108 suggest that the T cells of these particular elite controllers may be naturally resistant to HIV infe
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
115 pared with HIV-1-infected subjects including elite controllers, noncontrollers, and patients receivin
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
124 A subset of HIV-1-infected patients known as elite controllers or suppressors (ES) control the virus
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
130 that is upregulated in CD4(+) T cells from "elite controllers," potently inhibited CDK2-dependent ph
134 imental blockade of p21 in CD4+ T cells from elite controllers resulted in a marked increase of viral
136 Furthermore, CXCR5(+) CD4(+) T cells from elite controllers showed a stronger ex vivo capacity to
139 following primary infection and enriched in elite controllers, suggesting a critical role for these
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
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
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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