ライフサイエンスコーパス: proviral load

1 activity was correlated with a reduction in proviral load.

2 most samples tested and was correlated with proviral load.

3 creased viral antibody response and a higher proviral load.

4 D4 and non-CD4 fractions, as measured by the proviral load.

5 RII inversely correlated with the HTLV-I tax proviral load.

6 roviral load of HTLV-1 and those with a high proviral load.

7 to an increase or a decrease in equilibrium proviral load.

8 tion of the TCR clonal expansion with HTLV-I proviral load.

9 e effect of fratricide on HTLV-I equilibrium proviral load.

10 nuclear translocation is important for high proviral load.

11 roblast infections that harbor higher enFeLV proviral loads.

12 ct HIV-1 DNA in infant whole blood with high proviral loads.

13 eripheral blood mononuclear cells and HTLV-1 proviral loads.

14 Some mutant inoculation groups had altered proviral loads.

15 ted uninfected T cells, both at high and low proviral loads.

16 gnificantly suppressed HIV-1 replication and proviral loads.

17 d, splenic proviral load 5-fold, bone marrow proviral load 14-fold, and infected bone marrow cells 7-

18 ced acute plasma viral load 28-fold, splenic proviral load 5-fold, bone marrow proviral load 14-fold,

19 was peripheral blood mononuclear cell (PBMC) proviral load after virologic control at different ages.

20 Therefore, proviral load and antibody titers may be useful as predi

21 and, together with clinical data, including proviral load and CD4 and CD8 levels, were used to asses

22 hich is necessary for the maintenance of the proviral load and determines HTLV-1-associated myelopath

23 eraction that significantly determine HTLV-I proviral load and disease risk.

24 creased, which correlated inversely with the proviral load and host antibody response against viral p

25 Correlations between proviral load and markers of active HIV production (ie,

26 ons there was a positive association between proviral load and neoplasia (P = 0.009).

27 of HAM/TSP and reported decreases in HTLV-1 proviral load and neuroinflammatory markers, with clinic

28 luid is proportional to the amount of HTLV-I proviral load and the levels of HTLV-I tax mRNA expressi

29 Thymic proviral load and the number of viral p24 Gag-positive c

30 mphocyte (CTL) response to HTLV-1 limits the proviral load and the risk of associated inflammatory di

31 nt, perhaps the decisive determinant, of the proviral load and the risk of HAM/TSP.

32 the first evidence linking Hbz expression to proviral load and the survival of the virus-infected cel

33 In Env mRNA-LNP immunized rabbits, proviral load and viral gene expression were significant

34 mutated in pX ORF II fail to obtain typical proviral loads and antibody responses in a rabbit animal

35 Co-existing high proviral loads and virus-specific CD8 T cells are import

36 infected as measured by antibody responses, proviral load, and HTLV-1 p19 matrix antigen production

37 tion and promotes cell proliferation, a high proviral load, and persistence in vivo.

38 The 2 groups had a similar HTLV-1 proviral load, but there was a significant increase in c

39 HTLV-1 Env SU altered antibody responses and proviral loads, but do not prevent viral replication in

40 The high proviral load characteristic of HTLV-1-associated inflam

41 m than ARVs and has been shown to reduce HIV proviral loads, clinical trials are under way to test wh

42 sion of HTLV-I-specific CD8+ T cells, HTLV-I proviral load did not decrease.

43 er, peripheral-blood mononuclear cell (PBMC) proviral loads did not correlate with antibody responses

44 e proviral load of HTLV-I; however, when the proviral load exceeds a threshold level, HTLV-I-specific

45 l load showed that females and patients with proviral load >50,000 copies/10(6) peripheral blood mono

46 during chronic infection, even after HTLV-1 proviral load has reached its set point, and we estimate

47 that have been adapted to studies of HTLV-I proviral load, HTLV-I mRNA, and HTLV-I tax-specific CD8

48 we examined HTLV-I/II serostatus and HTLV-I proviral load in 2 groups of individuals with WB seroind

49 sured human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells from human T-

50 io of human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells to peripheral

51 Human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells were signific

52 However, the proviral load in cerebrospinal fluid has not been well i

53 s accounted for between 66% and 97% of total proviral load in five of the eight AIDS patients.

54 toxic T-lymphocyte responses and high HTLV-I proviral load in HAM/TSP.

55 The proviral load in human T cell lymphotropic virus type 1

56 l load and human T-lymphotropic virus type I proviral load in infected patients.

57 However, observations of high HTLV-I proviral load in patients with HTLV-I-associated myelopa

58 high human T-cell lymphotropic virus type I proviral load in patients with human T-cell lymphotropic

59 o epitopes were found to be linked with high proviral load in PBMC.

60 e measures of gait, quantification of HTLV-1 proviral load in peripheral blood mononuclear cells, and

61 hesis, we evaluated HTLV-I/II serostatus and proviral load in prospectively collected specimens from

62 red peripheral blood mononuclear cell (PBMC) proviral load in the absence of a correlative specific i

63 Despite progressive neurologic signs, the proviral load in tissues, including several regions of t

64 tative competitive PCR indicated higher PBMC proviral loads in ACH.1-inoculated rabbits.

65 A comparison of proviral loads in mesenteric lymph node and peripheral b

66 and quantitative competitive PCR showed the proviral loads in PBMC from ACH.p30(II)/p13(II)-infected

67 ed rabbits to be dramatically lower than the proviral loads in rabbits exposed to ACH.

68 romoters, and is critical for maintenance of proviral loads in rabbits.

69 ty of IFN-alpha14 to reduce both viremia and proviral loads in vivo suggests that it has strong poten

70 ld-type mice at 7 d postinfection (dpi), and proviral loads inversely correlated with a stronger CD8(

71 de that successful suppression of the HTLV-1 proviral load is associated with strong cytotoxic CD8+ l

72 that a major determinant of the equilibrium proviral load is the CD8+ T cell response to HTLV-1.

73 We quantified proviral load, level of tax, and APH-2 in a series of bl

74 uction, anti-HTLV-1 serologic responses, and proviral load levels were measured during infection.

75 hat inversely correlated with the HTLV-I tax proviral load, loss of Treg suppressor function, and esc

76 HTLV-I and -II proviral load may be lower in sexually acquired infectio

77 This high proviral load may increase genome toxicity, potentially

78 distinguishes between individuals with a low proviral load of HTLV-1 and those with a high proviral l

79 opical spastic paraparesis), by reducing the proviral load of HTLV-I; however, when the proviral load

80 mphocytes from individuals with a low HTLV-1 proviral load overexpressed a core group of nine genes w

81 Higher cerebrospinal fluid HTLV-1 proviral load (p = 0.01) was associated with thinner spi

82 A high proviral load predisposes to HTLV-1-associated diseases.

83 stics of individuals with low or high HTLV-1 proviral load (pVL), symptomatic disease, and the impact

84 Blood was drawn for HTLV-1 serology and proviral load (PVL).

85 f HTLV-1-infected cells in peripheral blood (proviral load [PVL]), possible interactions between PVL

86 < 0.05), the presence of HIV-infected cells (proviral load; R = 0.608; P < 0.05) and genetic segregat

87 actors that determine an individual's HTLV-1 proviral load remain uncertain.

88 Kaplan-Meier curves stratified by sex and proviral load showed that females and patients with prov

89 o results in increased viral replication and proviral loads, suggesting that HBZ and APH-2 modulate t

90 roduce greater reductions in HIV-1 viral and proviral loads than ART alone.

91 e human T lymphotropic virus (HTLV)-I or -II proviral load (VL) may be linked to viral pathogenesis,

92 HTLV-I or -II proviral load was 2 log10 lower in newly infected partne

93 Lower proviral load was associated with undetectable 2-long te

94 HIV-1 proviral load was determined by quantitative PCR in 65 o

95 ers (80% vs 20%; P = .03), and median HTLV-1 proviral load was greater in CT/TT than CC carriers (P =

96 In early infection, proviral load was initially elevated (median, 212 copies

97 Moreover, maternal proviral load was not associated with transmission, but

98 PBMC proviral load was significantly lower in ET youth (media

99 No associations with proviral load were observed.

100 Low proviral loads were detected in 42% of patients with neu

101 Proviral loads were similar in both study groups, peakin

102 ammatory disease is strongly correlated with proviral load, which in turn is correlated with the numb

103 ssion over time directly correlates with the proviral load, which provides the first evidence linking

104 ition of HIV-1 expression and a reduction in proviral load within macrophage cultures.