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1 ex, age, and HLA-DR who had not progressed ("nonprogressors").
2 maining four macaques remained asymptomatic (nonprogressors).
3 and did not progress to AIDS within 9-10 yr (nonprogressors).
4 in two well-defined groups (progressors vs. nonprogressors).
5 ith chronic HIV infection, and one long-term nonprogressor.
6 se mutations was found in more than a single nonprogressor.
7 volution patterns differ for progressors and nonprogressors.
8 ise periodically in HIV-1-infected long-term nonprogressors.
9 isit were both higher in progressors than in nonprogressors.
10 unodeficiency virus (HIV)-infected long-term nonprogressors.
11 attered over the CCR5 coding sequence from 8 nonprogressors.
12 tions was silent, and each was unique to two nonprogressors.
13 ower viral load compared with CCR5 wild-type nonprogressors.
14 racterized by a larger proportion of slow or nonprogressors.
15 nodeficiency virus type 1-infected long-term nonprogressors.
16 0.83-0.88) to discriminate progressors from nonprogressors.
17 ho progressed to tuberculosis disease and 15 nonprogressors.
18 D onset and distinguish T1D progressors from nonprogressors.
19 er progressed to tuberculosis or remained as nonprogressors.
20 -independent cohort of 13 progressors and 11 nonprogressors.
21 y virus infection as well as HIV-1 long-term nonprogressors.
22 in the minority of HIV-1-infected long-term nonprogressors.
23 ent dynamics were similar in progressors and nonprogressors.
24 oviral therapy-treated patients or long term nonprogressors.
25 s of multiple phospholipids as compared with nonprogressors.
26 lated in scarring progressors relative to in nonprogressors.
27 ienced liver disease progression and 23 were nonprogressors.
28 L most accurately identified progressors and nonprogressors.
29 red with both healthy controls and long-term nonprogressors.
30 ronic HIV-1-infected patients, and long-term nonprogressors.
31 surements in discriminating progressors from nonprogressors.
32 tiating progressors from normal subjects and nonprogressors.
33 risk scores to discriminate progressors from nonprogressors.
34 acute HIV-1 infection but not from long-term nonprogressors.
35 avoided for the majority of UC patients, the nonprogressors.
36 t much less frequently in aviremic long-term nonprogressors.
37 adiographic progressors with 60 radiographic nonprogressors.
38 ronically HIV-infected individuals and elite nonprogressors.
39 than previously observed in adult long-term nonprogressors.
40 icantly higher for progressors compared with nonprogressors (-0.72 mum/y vs. 0.14 mum/y; P = 0.004),
42 higher in the progressors compared with the nonprogressors (12.52 +/- 2.71 versus 10.82 +/- 2.71; P
43 higher in the progressors compared with the nonprogressors (14.12 +/- 3.39 units/liter versus 12.62
51 genotype was identified in 33 of 172 (19.2%) nonprogressors and 25 of 234 (10.7%) progressors from th
54 ht to clarify the role of beta-chemokines in nonprogressors and AIDS patients by examination of beta-
56 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons have h
57 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons, as we
59 omarkers can distinguish UC progressors from nonprogressors and improve cancer surveillance in UC.
60 patients but have been reported in long-term nonprogressors and in patients treated with highly activ
61 r results show that cocaine-using, long-term nonprogressors and normal progressors of HIV infection m
62 IGN compared with cocaine-nonusing long-term nonprogressors and normal progressors, respectively.
63 es (AUC) in differentiating progressors from nonprogressors and normal subjects were compared to the
64 ts showed no evidence of differences between nonprogressors and progressors (mean, -5.5 g/L +/- 9.5 v
65 of HIV-specific CD8+ T cells were present in nonprogressors and progressors, only those of nonprogres
67 d in human TB progressors when compared with nonprogressors and rapidly decreased S100A8/A9 protein l
71 It distinguished between progressors and nonprogressors and was associated with a greater decline
72 sequence (CCR5-Delta32) was found in 4 of 13 nonprogressors, and 12 different point mutations were fo
73 y more than two-fold between progressors and nonprogressors, and 12 miRs differed between late presen
74 nfection (clinical progressors), 10 clinical nonprogressors, and 3 immunologically discordant progres
77 ed that these patients, as well as long-term nonprogressors, are infected with defective HIV-1 varian
78 llowed for 7-20 years (rapid progressors and nonprogressors), as well as a reference panel of normoal
80 We further show that in a rare long-term nonprogressor, both an HIV-1-specific CD4(+)-T-cell clon
81 L2RA) did not differ between progressors and nonprogressors but were elevated in both groups relative
82 who had CD4 cell counts similar to those of nonprogressors but with a high likelihood of disease pro
86 tion of both progressor (BALB) and long term nonprogressor (C57BL) mouse strains is characterized by
87 4 down-modulation, and a subset of long-term nonprogressors carry viruses defective in this function.
88 clinical progressors (CDR score, >/=0.5) and nonprogressors (CDR score, 0) and between APOE epsilon4
90 ific proliferative responses in the clinical nonprogressor cohort that correlated with significant nu
91 is increased among HIV-1- infected long-term nonprogressors compared with progressors; however, the h
92 eristics were not different in this group of nonprogressors compared with those with low AIRg who did
94 istance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment
96 differed significantly in progressors versus nonprogressors (DQB*0302, 42.6 vs. 34.7%, P = 0.0047; DQ
98 in CD4(+) T cells from HIV-1 elite long-term nonprogressors (eLTNPs), naive patients, and multiply ex
100 y, B27- and B57-restricted CD8+ T cells from nonprogressors exhibited greater expansion than those re
101 se parameters from the progressors, the four nonprogressors exhibited more individual variability wit
102 utant identified in HIV-1-infected long-term nonprogressors failed to promote TERT destabilization.
104 sed genes was identified that distinguished "nonprogressors" from "progressors" with an estimated 100
107 plantation biopsies were classified as IF/TA nonprogressors (group 1) or progressors (group 2) using
109 , progressors had a higher risk category and nonprogressors had a lower risk category when genetic fa
111 lin G (IgG) from rapid progressors, IgG from nonprogressors had no suppressive effects on glycoprotei
113 d because genetic studies of long-term HIV-1 nonprogressors have associated specific HLA-B alleles wi
116 ) T cells in coinfected HLA-DR7(+) long-term nonprogressor HIV subjects with undetectable HCMV plasma
117 ) of 73% for distinguishing progressors from nonprogressors in a cohort of 596 individuals with knee
119 a community-based cohort of HIV-2 long-term nonprogressors in rural Guinea-Bissau, we performed what
120 ressed, no difference was seen compared with nonprogressors in spine BMD, but hip BMD was modestly re
121 asia (UC progressors) from those without (UC nonprogressors), including assays of telomere length, an
123 in intestinal mucosal biopsies of long-term nonprogressor (LTNP) patients as compared to chronically
124 ation in elite controller (EC) and long-term nonprogressor (LTNP) patients has been associated with e
127 lones from two progressors and two long-term nonprogressors (LTNP) in fetal thymic organ culture (FTO
128 -mediated control over HIV, termed long-term nonprogressors (LTNP) or elite controllers, and patients
129 A unique cohort of HIV-1-infected long term nonprogressors (LTNP) with normal CD4(+) T cell counts a
130 tetanus toxoid in normal controls, long-term nonprogressors (LTNP), and HIV-infected patients with pr
131 ed Rx <50) and untreated patients (long-term nonprogressors [LTNP]) matched for very low HIV RNA leve
133 ture by autologous CD8+ T cells in long-term nonprogressors (LTNPs) and in patients whose viremia was
137 V type 1-infected, untreated white long-term nonprogressors (LTNPs) with a cohort of 605 HIV-1-infect
138 an immunodeficiency virus (HIV) in long-term nonprogressors (LTNPs) with protective human leukocyte a
139 11 healthy donors, 360 +/- 69 in 3 long-term nonprogressors (LTNPs), 186 +/- 52 in 9 newly diagnosed
140 nts including typical progressors, long-term nonprogressors (LTNPs), and vertically HIV-infected subj
141 unodeficiency virus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expect
142 t been evaluated in HIV-1-infected long-term nonprogressors (LTNPs), who maintain high CD4(+) T cell
145 a lack of disease progression (ie, long-term nonprogressors [LTNPs]) through 7 years of follow-up (LT
149 onprogressors and progressors, only those of nonprogressors maintained a high proliferative capacity.
151 mean age, 72 years +/- 7; five women) and 13 nonprogressors (mean age, 70 years +/- 10; 11 men).
152 ral therapy (n = 21), HIV-infected long-term nonprogressors (n = 10), and HIV-seronegative volunteers
153 decline > 5 ml/min/1.73 m2/year, n = 23) or nonprogressors (n = 23)-and 23 healthy controls (HC) wer
154 gressors had lower baseline FPIR values than nonprogressors (n = 270), with adjustments made for age
156 = 63), elite controllers (n = 19), long-term nonprogressors (n = 7), and HIV-infected patients affect
158 "Progressors" (N = 41) did not differ from "nonprogressors" (N = 156) in terms of hours per day spen
159 diagnosis with BE were matched to controls (nonprogressors, n = 291), for age, sex, and year of BE d
162 ere classified as progressors (P = F0/F1) or nonprogressors (NP = F3/F4) according to the severity of
163 were compared: eight progressors (P) and 45 nonprogressors (NP), using Cox proportional hazards mode
164 classifier to differentiate progressors and nonprogressors on baseline cartilage texture maps, which
167 tuberculosis infection who remained healthy (nonprogressors) or who progressed to microbiologically c
171 nificantly over time between progressors and nonprogressors (P = .60), progressors had significantly
172 methylation in progressors 67.8% vs 96.7% in nonprogressors; P = 0.0001, z = 3.85, Wilcoxon rank-sum
173 cells from PBMCs from HIV-positive long-term nonprogressors; partial blocking of infection with chemo
174 endent manner, with discordant and long-term nonprogressor patients showing elevated SLAMF7 levels, a
175 PWH with CD4 count >200 cells/uL, long-term nonprogressors, people with idiopathic CD4 lymphopenia,
177 downregulation; how this contributes to the nonprogressor phenotype of these infected individuals re
180 rts of HIV-1-infected individuals: long-term nonprogressors, progressors to disease, acute seroconver
181 ogression and treatment, including long-term nonprogressors, progressors, and chronically infected su
182 apid progressors and nonrapid progressors or nonprogressors remained when longitudinal changes within
183 biopsy samples from long-term HIV-1-infected nonprogressors showed maintenance of normal CD4(+) T-cel
184 progressor phenotype are akin to MM, whereas nonprogressor SMM has monoclonal gammopathy of undetermi
188 mechanisms by which long-term HIV-1-infected nonprogressors suppress HIV-1 infection and maintain imm
190 seen in HIV elite controllers and long-term nonprogressors that does not require combined antiretrov
191 differ between liver disease progressors and nonprogressors, the association of sCD14, I-FABP, and IL
193 , in a cohort of 33 HIV-1-infected long-term nonprogressors, those who were heterozygous for the muta
194 aseline NAS between fibrosis progressors and nonprogressors, though NAS rose over time in the progres
195 ed in unrelated cohorts (including long-term nonprogressors), thus confirming their independence from
199 ould be correctly assigned as progressors or nonprogressors using random sample cross-validation stat
201 ost striking attribute of long-term survivor nonprogressors was the detection of HIV-1-specific CD4(+
202 dly, biologic clones from an adult long-term nonprogressor were noncytopathic in spite of similar lev
203 0.86 and in differentiating progressors from nonprogressors were 0.68 and 0.64, respectively; the AUC
204 The mean +/- SD ages of the progressors and nonprogressors were 64.2 +/- 7.8 years and 63.3 +/- 10.6
210 on to beta-chemokine production; clones from nonprogressors were poorly susceptible to ADA replicatio
214 n progressors is limited compared to that of nonprogressors, who consistently maintain highly functio
215 low-up and were selected as progressors; 106 nonprogressors, who remained healthy, were matched to pr
216 mutant CCR5 gene might define a subgroup of nonprogressors with higher CD4+ T cell counts and lower
217 ere secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated.
218 udied including a unique cohort of long-term nonprogressors with low levels of plasma viral RNA and s
219 tion favoring nonsynonymous mutations, while nonprogressors with low viral loads selected against the
221 e were indistinguishable from CCR5 wild-type nonprogressors with regard to all measured immunologic a
224 y was lower in T1D progressors compared with nonprogressors, with simultaneous lower diglycerides, ly
225 cer/dysplasia and/or aneuploidy) compared to nonprogressors (without cancer/dysplasia/aneuploidy), wh