ライフサイエンスコーパス: LTNP

1 LTNP patients had undetectable viral loads, normal CD4+

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

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

4 LTNPs had expansion of CD8 T cells with increased expres

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

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

7 blood mononuclear cells and lymph nodes of 3 LTNPs.

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

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

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

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

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

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

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

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

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

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

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

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

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

21 Both LTNPs maintained robust immune responses, including simi

22 We used longitudinal methods to characterise LTNP.

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

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

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

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

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

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

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

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

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

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

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

34 Sera from LTNPs had higher average titers of neutralizing antibodi

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

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

37 primary infection and are uniquely broad in LTNP.

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

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

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

41 elated positively in progressors, but not in LTNP.

42 0 was not restored to the levels observed in LTNP despite prolonged suppression of HIV RNA levels, pe

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

44 ferate to HIV antigens was preserved only in LTNP.

45 profiles correlate with clinical outcome in LTNP patients.

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

47 In LTNPs with chronic infection, the colon had consistently

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

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

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

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

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

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

54 be sufficient to establish superinfection in LTNPs.

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

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

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

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

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

60 d peripheral blood mononuclear cells of most LTNPs.

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

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

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

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

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

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

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

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

69 /10-H-2(k) (B10.BR) long-term nonprogressor (LTNP) mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 fic lymphoproliferation was vigorous in some LTNPs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Most individuals with LTNP eventually lose immunological and clinical control