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1 maining four macaques remained asymptomatic (nonprogressors).
2 and did not progress to AIDS within 9-10 yr (nonprogressors).
3  in two well-defined groups (progressors vs. nonprogressors).
4 ith chronic HIV infection, and one long-term nonprogressor.
5 se mutations was found in more than a single nonprogressor.
6 volution patterns differ for progressors and nonprogressors.
7  in the minority of HIV-1-infected long-term 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 ent dynamics were similar in progressors and nonprogressors.
14 ower viral load compared with CCR5 wild-type nonprogressors.
15 nodeficiency virus type 1-infected long-term nonprogressors.
16 oviral therapy-treated patients or long term nonprogressors.
17 s of multiple phospholipids as compared with nonprogressors.
18 ienced liver disease progression and 23 were nonprogressors.
19 L most accurately identified progressors and nonprogressors.
20 red with both healthy controls and long-term nonprogressors.
21 ronic HIV-1-infected patients, and long-term nonprogressors.
22 racterized by a larger proportion of slow or nonprogressors.
23 surements in discriminating progressors from nonprogressors.
24 tiating progressors from normal subjects and nonprogressors.
25 risk scores to discriminate progressors from nonprogressors.
26 acute HIV-1 infection but not from long-term nonprogressors.
27 avoided for the majority of UC patients, the nonprogressors.
28 t much less frequently in aviremic long-term nonprogressors.
29 D onset and distinguish T1D progressors from nonprogressors.
30 adiographic progressors with 60 radiographic nonprogressors.
31 ronically HIV-infected individuals and elite nonprogressors.
32  than previously observed in adult long-term nonprogressors.
33 y virus infection as well as HIV-1 long-term nonprogressors.
34 icantly higher for progressors compared with nonprogressors (-0.72 mum/y vs. 0.14 mum/y; P = 0.004),
35 ial overlap between the two groups (range of nonprogressors, 0.10-1.7%).
36  higher in the progressors compared with the nonprogressors (12.52 +/- 2.71 versus 10.82 +/- 2.71; P
37  higher in the progressors compared with the nonprogressors (14.12 +/- 3.39 units/liter versus 12.62
38  rapid progressors to AIDS (24 patients) and nonprogressors (47 controls).
39    Progressors were significantly older than nonprogressors (70.6 versus 62.5 years; P < 0.001).
40                                    Long-term nonprogressor AD-18 has been infected with human immunod
41                                              Nonprogressors also had decreased BCHE activity over tim
42             The high proportion of long-term nonprogressors among chronic lymphocytic leukemia (CLL)
43 genotype was identified in 33 of 172 (19.2%) nonprogressors and 25 of 234 (10.7%) progressors from th
44               Methylation was assayed in 145 nonprogressors and 50 progressors using real-time quanti
45 progressors was readily separable from 15 UC nonprogressors and 6 normal controls.
46 ht to clarify the role of beta-chemokines in nonprogressors and AIDS patients by examination of beta-
47                             CD4+ clones from nonprogressors and CD8+ clones from AIDS patients secret
48 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons have h
49 Immunologic and genetic studies of long-term nonprogressors and exposed yet uninfected persons, as we
50                                Both clinical nonprogressors and immunologically discordant progressor
51 omarkers can distinguish UC progressors from nonprogressors and improve cancer surveillance in UC.
52 patients but have been reported in long-term nonprogressors and in patients treated with highly activ
53 r results show that cocaine-using, long-term nonprogressors and normal progressors of HIV infection m
54 IGN compared with cocaine-nonusing long-term nonprogressors and normal progressors, respectively.
55 es (AUC) in differentiating progressors from nonprogressors and normal subjects were compared to the
56 of HIV-specific CD8+ T cells were present in nonprogressors and progressors, only those of nonprogres
57 ogous isolate than were sera from short-term nonprogressors and progressors.
58 gressive HIV disease compared with long-term nonprogressors and responders.
59                             Lymphocytes from nonprogressors and seronegative controls also showed neg
60                 Twenty biopsies from four UC nonprogressors and twenty-one biopsies from control indi
61 sequence (CCR5-Delta32) was found in 4 of 13 nonprogressors, and 12 different point mutations were fo
62 y more than two-fold between progressors and nonprogressors, and 12 miRs differed between late presen
63 nfection (clinical progressors), 10 clinical nonprogressors, and 3 immunologically discordant progres
64                     HIV-1-infected long-term nonprogressors are a heterogeneous group of individuals
65 re their third birthday (>89%) and long-term nonprogressors are rare.
66 ed that these patients, as well as long-term nonprogressors, are infected with defective HIV-1 varian
67 llowed for 7-20 years (rapid progressors and nonprogressors), as well as a reference panel of normoal
68 gressors at corresponding visits or those of nonprogressors at any visit.
69     We further show that in a rare long-term nonprogressor, both an HIV-1-specific CD4(+)-T-cell clon
70 L2RA) did not differ between progressors and nonprogressors but were elevated in both groups relative
71  who had CD4 cell counts similar to those of nonprogressors but with a high likelihood of disease pro
72  years were compared between progressors and nonprogressors by Student's 2-tailed t-test.
73 ), while 265 children remained disease free (nonprogressors) by December 2011.
74 tion of both progressor (BALB) and long term nonprogressor (C57BL) mouse strains is characterized by
75 4 down-modulation, and a subset of long-term nonprogressors carry viruses defective in this function.
76 clinical progressors (CDR score, >/=0.5) and nonprogressors (CDR score, 0) and between APOE epsilon4
77              In comparison with HIV-positive nonprogressor chimpanzees, progressors have higher plasm
78 ific proliferative responses in the clinical nonprogressor cohort that correlated with significant nu
79 is increased among HIV-1- infected long-term nonprogressors compared with progressors; however, the h
80 eristics were not different in this group of nonprogressors compared with those with low AIRg who did
81 istance to ADA infection in CD4+ clones from nonprogressors could be partially reversed by treatment
82 differed significantly in progressors versus nonprogressors (DQB*0302, 42.6 vs. 34.7%, P = 0.0047; DQ
83 activity was observed in sera from long-term nonprogressors (elite controllers).
84 in CD4(+) T cells from HIV-1 elite long-term nonprogressors (eLTNPs), naive patients, and multiply ex
85 atients and discusses them in the context of nonprogressors enrolled in other cohorts.
86 y, B27- and B57-restricted CD8+ T cells from nonprogressors exhibited greater expansion than those re
87 se parameters from the progressors, the four nonprogressors exhibited more individual variability wit
88 utant identified in HIV-1-infected long-term nonprogressors failed to promote TERT destabilization.
89 sed genes was identified that distinguished "nonprogressors" from "progressors" with an estimated 100
90                                              Nonprogressors generally had high titers of ADCC Abs at
91 plantation biopsies were classified as IF/TA nonprogressors (group 1) or progressors (group 2) using
92 NS DNA in the at-risk progressor and at-risk nonprogressor groups followed for 4 years.
93                  Although long-term survivor nonprogressors had a significantly higher percentage of
94 lin G (IgG) from rapid progressors, IgG from nonprogressors had no suppressive effects on glycoprotei
95                          Patients defined as nonprogressors had significantly lower baseline levels o
96 d because genetic studies of long-term HIV-1 nonprogressors have associated specific HLA-B alleles wi
97                                    Long-term nonprogressors have high titer antibody responses to HIV
98 ) T cells in coinfected HLA-DR7(+) long-term nonprogressor HIV subjects with undetectable HCMV plasma
99 ells are elevated in blood of HIV+ long-term nonprogressors in comparison to HIV- donors.
100  a community-based cohort of HIV-2 long-term nonprogressors in rural Guinea-Bissau, we performed what
101 ressed, no difference was seen compared with nonprogressors in spine BMD, but hip BMD was modestly re
102 asia (UC progressors) from those without (UC nonprogressors), including assays of telomere length, an
103 r (P) and C57BL/10-H-2(k) (B10.BR) long-term nonprogressor (LTNP) mice.
104  in intestinal mucosal biopsies of long-term nonprogressor (LTNP) patients as compared to chronically
105 ation in elite controller (EC) and long-term nonprogressor (LTNP) patients has been associated with e
106                                    Long-term nonprogressors (LTNP) and seronegative controls had leve
107                Undiluted sera from long-term nonprogressors (LTNP) had broad neutralizing antibodies
108 lones from two progressors and two long-term nonprogressors (LTNP) in fetal thymic organ culture (FTO
109 -mediated control over HIV, termed long-term nonprogressors (LTNP) or elite controllers, and patients
110  A unique cohort of HIV-1-infected long term nonprogressors (LTNP) with normal CD4(+) T cell counts a
111 tetanus toxoid in normal controls, long-term nonprogressors (LTNP), and HIV-infected patients with pr
112 ed Rx <50) and untreated patients (long-term nonprogressors [LTNP]) matched for very low HIV RNA leve
113 jects; the latter group included 8 long-term nonprogressors (LTNPs) and 17 progressors.
114 ture by autologous CD8+ T cells in long-term nonprogressors (LTNPs) and in patients whose viremia was
115                              Seven long-term nonprogressors (LTNPs) have been identified in a cohort
116                                    Long-term nonprogressors (LTNPs) of human immunodeficiency virus t
117 cation in rare individuals, termed long-term nonprogressors (LTNPs) or elite controllers.
118 V type 1-infected, untreated white long-term nonprogressors (LTNPs) with a cohort of 605 HIV-1-infect
119 an immunodeficiency virus (HIV) in long-term nonprogressors (LTNPs) with protective human leukocyte a
120 11 healthy donors, 360 +/- 69 in 3 long-term nonprogressors (LTNPs), 186 +/- 52 in 9 newly diagnosed
121 nts including typical progressors, long-term nonprogressors (LTNPs), and vertically HIV-infected subj
122 unodeficiency virus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expect
123 t been evaluated in HIV-1-infected long-term nonprogressors (LTNPs), who maintain high CD4(+) T cell
124                               True long-term nonprogressors (LTNPs)/elite controllers (ECs) maintain
125 a lack of disease progression (ie, long-term nonprogressors [LTNPs]) through 7 years of follow-up (LT
126                     Here we tested long-term nonprogressors' (LTNPs') susceptibility to superinfectio
127 unodeficiency virus (SIV)-infected long-term-nonprogressor macaque.
128                            Compared with the nonprogressor macaques, the two progressor macaques exhi
129 onprogressors and progressors, only those of nonprogressors maintained a high proliferative capacity.
130 ns with progressive disease, suggesting that nonprogressors may not target unique epitopes.
131 ral therapy (n = 21), HIV-infected long-term nonprogressors (n = 10), and HIV-seronegative volunteers
132 gressors had lower baseline FPIR values than nonprogressors (n = 270), with adjustments made for age
133 = 63), elite controllers (n = 19), long-term nonprogressors (n = 7), and HIV-infected patients affect
134 were stratified as progressors (n = 200) and nonprogressors (n = 751) and compared.
135  "Progressors" (N = 41) did not differ from "nonprogressors" (N = 156) in terms of hours per day spen
136  diagnosis with BE were matched to controls (nonprogressors, n = 291), for age, sex, and year of BE d
137   All others were considered nonprogressing (nonprogressors; n = 210 eyes).
138                Thus, in contrast to clinical nonprogressors, neither progressors nor immunologically
139 ere classified as progressors (P = F0/F1) or nonprogressors (NP = F3/F4) according to the severity of
140  were compared: eight progressors (P) and 45 nonprogressors (NP), using Cox proportional hazards mode
141  seen in HIV-1-infected cohorts of long-term nonprogressors or patients with AIDS.
142                                    Long-term nonprogressors or slow progressors may remain asymptomat
143 s/y in progressors versus -8,808 cells/y for nonprogressors (P < 0.001).
144 in progressors versus an increase of 0.6% in nonprogressors (P < 0.05).
145 brosis progressors compared with 20 fibrosis nonprogressors (P < 0.05).
146 nificantly over time between progressors and nonprogressors (P = .60), progressors had significantly
147 cells from PBMCs from HIV-positive long-term nonprogressors; partial blocking of infection with chemo
148                      In studies of long-term nonprogressors - persons who have stable CD4+ T-cell cou
149  downregulation; how this contributes to the nonprogressor phenotype of these infected individuals re
150 rts of HIV-1-infected individuals: long-term nonprogressors, progressors to disease, acute seroconver
151 ogression and treatment, including long-term nonprogressors, progressors, and chronically infected su
152 apid progressors and nonrapid progressors or nonprogressors remained when longitudinal changes within
153 biopsy samples from long-term HIV-1-infected nonprogressors showed maintenance of normal CD4(+) T-cel
154 tion in Vif contributes significantly to the nonprogressor status of this mother and child.
155 decrease virus burden, whereas the long term nonprogressor strains do not.
156 esions from each of ten progressors and four nonprogressors suffering from longstanding UC.
157 mechanisms by which long-term HIV-1-infected nonprogressors suppress HIV-1 infection and maintain imm
158 differ between liver disease progressors and nonprogressors, the association of sCD14, I-FABP, and IL
159                                           In nonprogressors, the myopia progression at 1 year was les
160 , in a cohort of 33 HIV-1-infected long-term nonprogressors, those who were heterozygous for the muta
161 ort Study, enriched with rapid and long-term nonprogressors to increase statistical power.
162 ould be correctly assigned as progressors or nonprogressors using random sample cross-validation stat
163              However, IL-4 production in the nonprogressors was restricted to a limited number of p24
164 ost striking attribute of long-term survivor nonprogressors was the detection of HIV-1-specific CD4(+
165 dly, biologic clones from an adult long-term nonprogressor were noncytopathic in spite of similar lev
166 0.86 and in differentiating progressors from nonprogressors were 0.68 and 0.64, respectively; the AUC
167  The mean +/- SD ages of the progressors and nonprogressors were 64.2 +/- 7.8 years and 63.3 +/- 10.6
168                           Progressors versus nonprogressors were compared using the two-sample t-test
169                 These results indicated that nonprogressors were differentiated by increased prolifer
170                                     Clinical nonprogressors were found to respond to a wide range of
171 on to beta-chemokine production; clones from nonprogressors were poorly susceptible to ADA replicatio
172       The recent discovery of long term AIDS nonprogressors who harbor nef-attenuated HIV suggests th
173                         We hypothesized that nonprogressors who were heterozygous for the mutant CCR5
174             An estimated 25-30% of long-term nonprogressors (who avoid clinical AIDS for 10 or more y
175 n progressors is limited compared to that of nonprogressors, who consistently maintain highly functio
176  mutant CCR5 gene might define a subgroup of nonprogressors with higher CD4+ T cell counts and lower
177 ere secreted when CD8 T cells from long-term nonprogressors with HIV-1 infection were stimulated.
178 udied including a unique cohort of long-term nonprogressors with low levels of plasma viral RNA and s
179 tion favoring nonsynonymous mutations, while nonprogressors with low viral loads selected against the
180 cificity for distinguishing progressors from nonprogressors with optimum choice of threshold.
181 e were indistinguishable from CCR5 wild-type nonprogressors with regard to all measured immunologic a
182 c CD8+ T cells were not limited to long-term nonprogressors with restriction of plasma virus.
183                       Furthermore, long-term nonprogressors with the wild-type CCR5 genotype are indi
184 cer/dysplasia and/or aneuploidy) compared to nonprogressors (without cancer/dysplasia/aneuploidy), wh

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