ライフサイエンスコーパス: LTNP

1 LTNP patients had undetectable viral loads, normal CD4+

2 LTNP reduced aflatoxin contamination to levels below all

3 LTNP-C showed lower plasma IP-10 (p=0.019) and higher IF

4 LTNPs defined by 10-year versus 7-year criteria had a lo

5 LTNPs had expansion of CD8 T cells with increased expres

6 virus sequences in 27 B(*)57(+) patients (10 LTNPs and 17 progressors).

7 ls in 31 HIV controller patients (15 ECs, 16 LTNPs).

8 blood mononuclear cells and lymph nodes of 3 LTNPs.

9 cell responses were observed between B*57(+) LTNP and five B*57(+) progressors (P = 0.4).

10 cific responses that distinguish HLA B*57(+) LTNP from progressors may ultimately define mechanisms o

11 he differential abilities of HLA B(*)5701(+) LTNPs and progressors to restrict virus replication.

12 ood sorted resting CD4 T-cell subsets from 8 LTNPs with and 10 without HLA-B*27 or HLA-B*57 alleles (

13 unctions were down-regulated in both HVL and LTNP patients.

14 mice, immunosuppressed mice from both P and LTNP strains develop lymphomas about 2 months after infe

15 In our studies, however, both P and LTNP strains produce similar titers of neutralizing and

16 (IL-2), IL-4, and IL-7, both progressor and LTNP clones exhibited similar replication and CPE, which

17 Definitions of controllers and LTNPs describe distinct populations whose differing clin

18 rates (vertically HIV-infected patients and LTNPs, including HIV controllers) had significantly high

19 In HLA-B27/B57 LTNPs, a lower activation level of their memory CD4 T ce

20 The best LTNP combinations achieved aflatoxin exposure reduction

21 HCV was not significantly different between LTNP and progressors, even though their capacity to prol

22 ted with mitogens, the lymphocytes from both LTNP and progressors displayed indistinguishable levels

23 Both LTNPs maintained robust immune responses, including simi

24 We used longitudinal methods to characterise LTNP.

25 Long Term Non-Progressor HIV-1-controllers ((LTNP-C), defined by maintaining CD4(+)T-cells counts >50

26 Long Term Non-Progressor HIV-1-controllers ((LTNP-C), defined by maintaining CD4(+)T-cells counts >50

27 d and gut mucosa of HIV-uninfected controls, LTNPs, and HIV-1-infected individuals treated with prolo

28 persons who were distinct from conventional LTNPs/ECs in that they had extraordinarily low HIV burde

29 We defined LTNP as non-progression during the first 10 years after

30 and miR-155-5p can substantially distinguish LTNP individuals from regular progressors.

31 In addition, peripheral NK cells from EC/LTNP had increased NKG2D expression, significant HLA-DR

32 More importantly, EC/LTNP failed to induce expression of NKp44, a receptor ef

33 Thus, NK cells in EC/LTNP can maintain substantially unchanged functional cap

34 In EC/LTNP, induction of NKp46 expression was normal but short

35 isolates was equally prevalent for sera from LTNPs and non-LTNPs.

36 Sera from LTNPs had higher average titers of neutralizing antibodi

37 All viruses from LTNPs had a non-syncytium-inducing phenotype, were resis

38 ince HIV seroconversion, 283 individuals had LTNP, of whom 202 subsequently lost this status (median

39 primary infection and are uniquely broad in LTNP.

40 expansions of CMV-specific CD8(+) T cells in LTNP and progressors by increasing both the numbers of c

41 ricted cells is specific to HIV infection in LTNP and is not a feature of responses to other chronic

42 ns an important target of HIV-1 infection in LTNP, and these effects may ultimately contribute toward

43 elated positively in progressors, but not in LTNP.

44 0 was not restored to the levels observed in LTNP despite prolonged suppression of HIV RNA levels, pe

45 restored in Rx <50 to the level observed in LTNP, even though HIV-specific CD4+ T-cell proliferation

46 ferate to HIV antigens was preserved only in LTNP.

47 profiles correlate with clinical outcome in LTNP patients.

48 The HIV-specific CD4+ T-cell responses in LTNP and patients on therapy were similar in frequency,

49 In LTNPs with chronic infection, the colon had consistently

50 In LTNPs, T(CM) protection was correlated with preservation

51 no evidence of higher monocyte activation in LTNPs than in HIV-infected (HIV(-)) controls.

52 on, but not reaching the low levels found in LTNPs.

53 CTL precursor frequencies were higher in LTNPs than in patients with progressive disease.

54 variants caused breakthrough replication in LTNPs, although they readily infected Mamu-B 17-negative

55 arge intestine is a major viral reservoir in LTNPs, which may be the result of persistent, latently i

56 be sufficient to establish superinfection in LTNPs.

57 se with long-term, nonprogressive infection (LTNPs) usually have undetectable viremia, virus persists

58 mian immunodeficiency virus (SIV) infection, LTNPs preserve the balance of CD4(+) T cell populations

59 overed that the order of hA3G mRNA levels is LTNPs > HIV-uninfected subjects > progressors.

60 The MHC LTNP-associated SNPs are ordered in >/=4 linkage disequi

61 Moreover, LTNP-C exhibited higher quantities of IL2(+)CD57(-) and

62 d peripheral blood mononuclear cells of most LTNPs.

63 llular contact in patients who are naturally LTNPs or in those who are treated with HAART.

64 esented independent factors for becoming non-LTNP-C (TT/TT, ss469415590, OR=0.401 (0.171-0.942) p=0.0

65 esented independent factors for becoming non-LTNP-C (TT/TT, ss469415590, OR=0.401 (0.171-0.942) p=0.0

66 s (p=0.002 and 0.041, respectively) than non-LTNP-C.

67 an 7 years after HIV-1 diagnosis) versus non-LTNP-C, who developed CD4(+)T-cells counts <500 cells/mm

68 an 7 years after HIV-1 diagnosis) versus non-LTNP-C, who developed CD4(+)T-cells counts <500 cells/mm

69 ed long-term non-progressors (LTNPs) and non-LTNPs were evaluated for virus neutralization and infect

70 qually prevalent for sera from LTNPs and non-LTNPs.

71 /10-H-2(k) (B10.BR) long-term nonprogressor (LTNP) mice.

72 mucosal biopsies of long-term nonprogressor (LTNP) patients as compared to chronically HIV-1-infected

73 controller (EC) and long-term nonprogressor (LTNP) patients has been associated with efficient CD8(+)

74 Long-term nonprogressors (LTNP) and seronegative controls had levels of spontaneou

75 ndiluted sera from long-term nonprogressors (LTNP) had broad neutralizing antibodies against heterolo

76 rogressors and two long-term nonprogressors (LTNP) in fetal thymic organ culture (FTOC) with and with

77 l over HIV, termed long-term nonprogressors (LTNP) or elite controllers, and patients with progressiv

78 of HIV-1-infected long term nonprogressors (LTNP) with normal CD4(+) T cell counts and <50 copies/ml

79 n normal controls, long-term nonprogressors (LTNP), and HIV-infected patients with progressive diseas

80 r group included 8 long-term nonprogressors (LTNPs) and 17 progressors.

81 us CD8+ T cells in long-term nonprogressors (LTNPs) and in patients whose viremia was controlled by h

82 Seven long-term nonprogressors (LTNPs) have been identified in a cohort of 128 human imm

83 Long-term nonprogressors (LTNPs) of human immunodeficiency virus type 1 (HIV-1) in

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

85 d, untreated white long-term nonprogressors (LTNPs) with a cohort of 605 HIV-1-infected white serocon

86 ncy virus (HIV) in long-term nonprogressors (LTNPs) with protective human leukocyte antigen (HLA) all

87 s, 360 +/- 69 in 3 long-term nonprogressors (LTNPs), 186 +/- 52 in 9 newly diagnosed patients, and 18

88 pical progressors, long-term nonprogressors (LTNPs), and vertically HIV-infected subjects were analyz

89 rus (HIV)-infected long-term nonprogressors (LTNPs), it is also present at the expected frequency (11

90 in HIV-1-infected long-term nonprogressors (LTNPs), who maintain high CD4(+) T cell counts and suppr

91 el of HIV-infected long-term nonprogressors (LTNPs).

92 True long-term nonprogressors (LTNPs)/elite controllers (ECs) maintain durable control

93 ntreated patients (long-term nonprogressors [LTNP]) matched for very low HIV RNA levels were comprehe

94 e progression (ie, long-term nonprogressors [LTNPs]) through 7 years of follow-up (LTNP7s; prevalence

95 Here we tested long-term nonprogressors' (LTNPs') susceptibility to superinfection using Indian rh

96 hat R5 HIV-1 clones from progressors but not LTNP were cytopathic in untreated FTOC.

97 that most clearly distinguished the cells of LTNP from those of Rx <50.

98 on was independently associated with loss of LTNP status (p = 0.009).

99 In univariable analyses, loss of LTNP status was associated with CD4 cell count at 10 yea

100 In the multivariable analyses, loss of LTNP status was associated with lower CD4 counts at 10 y

101 t to HIV-specific CD8(+) T-cell responses of LTNP, HLA B5701-restricted responses within CMV pp65 wer

102 per-cell basis, HIV-specific CD8+ T cells of LTNPs efficiently eliminated primary autologous HIV-infe

103 e observed that HIV-specific CD8+ T cells of LTNPs persisted at higher frequencies than those of trea

104 ated with some immunovirological features of LTNPs that may improve the outcome of future interventio

105 all (jejunum) and large (colon) intestine of LTNPs.

106 mmune preservation (CD4/CD8), reminiscent of LTNPs, were found in early compared to late-treated pati

107 has been demonstrated in previous studies of LTNPs/ECs.

108 Viruses of LTNPs exhibited slow growth in vivo and in vitro.

109 efficacy of low-temperature nitrogen plasma (LTNP) in destroying fungi and reducing exposure to aflat

110 m to serially challenge 2 Mamu-B 17-positive LTNPs.

111 ated with loss of long-term non-progression (LTNP) status.

112 human PBMCs from long term non progressors (LTNPs), regular progressors and rapid progressors.

113 (HIV-1)-infected long-term non-progressors (LTNPs) and non-LTNPs were evaluated for virus neutraliza

114 roconverters, and long-term non-progressors (LTNPs) who have spontaneous virological control without

115 than those seen in seven carefully selected LTNPs were commonly observed in specimens collected soon

116 cation in the latent viral reservoir in some LTNPs and patients receiving HAART, but not in chronical

117 fic lymphoproliferation was vigorous in some LTNPs.

118 progressors replicated to higher levels than LTNP-derived R5 HIV-1 clones in this system.

119 evident prior to CD4 T cell decline and that LTNP are relatively resistant to the factors that induce

120 We found that LTNPs have intact CD4(+) T cell populations, including T

121 We found that LTNPs have substantial lower expression of miR-382-5p th

122 plications, these data support the idea that LTNPs may be a pathophysiologically distinct subgroup am

123 Results indicate that LTNPs produce vigorous serum antibody responses and that

124 enetic locus that may be responsible for the LTNP trait.

125 e gag-specific CD8(+) T cell response in the LTNP group was highly focused on peptides previously sho

126 + MuLV infection, it is more likely that the LTNP phenotype in E-55+ MuLV-infected mice is regulated

127 bone marrow chimeras to demonstrate that the LTNP phenotype is associated with the genotype of donor

128 months after infection, indicating that the LTNP phenotype is determined by the immune response of t

129 by the rs9368699 SNP) seems specific to the LTNP phenotype.

130 ation (false discovery rate, <0.05) with the LTNP condition, among which 5 reached genome-wide signif

131 A-B*57 was independently associated with the LTNP-C phenotype (OR=3.056 (1.029-9.069) p=0.044 and OR=

132 A-B*57 was independently associated with the LTNP-C phenotype (OR=3.056 (1.029-9.069) p=0.044 and OR=

133 However, only the LTNPs were able to stably maintain such an efficient vir

134 Thus, LTNPs in this cohort have maintained remarkably low viru

135 stinal mucosa of HVL patients as compared to LTNP patients.

136 unique cases were distinguished from typical LTNPs/ECs based on weakly reactive Western blots, undete

137 As a group, typical LTNPs/ECs have unequivocally reactive HIV-1 Western blot

138 ut comparatively lower than those of typical LTNPs/ECs.

139 Responses were correlated with LTNP status and CD4 cell count.

140 Most individuals with LTNP eventually lose immunological and clinical control