ライフサイエンスコーパス: viral burden

1 ups had comparable immune-reconstitution and viral burden.

2 esting a mechanism to explain this increased viral burden.

3 lso responded to IL-2 resulting in decreased viral burden.

4 al infection while also functioning to limit viral burden.

5 tively infected and contributed to the local viral burden.

6 cally accounted for over 90% of the cellular viral burden.

7 found to harbor less than 1% of the cellular viral burden.

8 and around inflammatory infiltrates and not viral burden.

9 nodes and peripheral blood is a function of viral burden.

10 d be a surrogate marker for a high pulmonary viral burden.

11 hocytic alveolitis reflects a high pulmonary viral burden.

12 the OI-induced pathology, but also limit the viral burden.

13 se transcriptase inhibitors markedly reduced viral burden.

14 depletion of CD4+ thymocytes, apoptosis, and viral burden.

15 whereby IFN-alpha therapy results in reduced viral burden.

16 rganism, leading to a reduction in its total viral burden.

17 ession of AIDS, CD4+ or CD8+ cell counts, or viral burden.

18 s of such therapy on both CD4 counts and the viral burden.

19 ion and the inability of the host to control viral burden.

20 gher levels of proinflammatory cytokines and viral burden.

21 lone-13 infection exhibited by mortality and viral burden.

22 a in a STAT4-dependent manner to limit early viral burden.

23 ls, with minimal effect on the intracellular viral burden.

24 arly Gag-responsive CD4 events are shaped by viral burden.

25 8(+) T cells was ineffective at reducing the viral burden.

26 usted virus-specific CD8 T cells and reduced viral burden.

27 loproteinases is equally crucial in lowering viral burden.

28 tide in this region were associated with low viral burden.

29 ncy, and its absence results in an increased viral burden.

30 cells were noted in patients with the higher viral burdens.

31 sm in the brain, as well as the relative CNS viral burdens.

32 superinfection had no significant effect on viral burdens.

33 s 4.4 months; P = .06) and higher cumulative viral burden (14.2 vs 12.5 log EBV copies/mL; P = .06).

34 n are more likely to have a lower total body viral burden, a homogenous viral population, and preserv

35 cosal lamina propria, thereby decreasing the viral burden, access to susceptible cells, and the chron

36 The reduced viral burden achieved solely with an env-based vaccine s

37 Viral burdens achieved by the two nonneurovirulent virus

38 immunized, immunized animals had a decreased viral burden after challenge with infectious virus, more

39 rovided only modest, transient reductions in viral burden after challenge with virulent, pathogenic S

40 oduction, which in turn increased epithelial viral burden, airway smooth muscle growth, and type 2 in

41 ugh mice lacking RNase L showed a higher CNS viral burden and an increased mortality, they were less

42 continued to have decreased cell-associated viral burden and another subject had more than doubled C

43 ure treatment with MAb 201 can alleviate the viral burden and associated pathological findings in a g

44 ols WNV infection by restricting tropism and viral burden and by preventing death of infected neurons

45 The inverse relationship between viral burden and DAT availability further supports HIV-m

46 deficient mice had greater mortality, higher viral burden and defective type I interferon response co

47 that influence the risk of HIV transmission, viral burden and disease progression.

48 he importance of tissue macrophages in local viral burden and further implicate roles for CC chemokin

49 H1N1 infection, potentially owing to greater viral burden and impaired Treg function, may be a novel

50 ure occurs under favorable conditions of low viral burden and in the absence of ongoing high level cy

51 ted mice with recombinant IL-17A reduces the viral burden and increases survival of mice, suggesting

52 y 6 postinfection, significantly reduces the viral burden and increases survival, suggesting a therap

53 bility of cytotoxic T lymphocytes to control viral burden and influence the outcome of disease, are p

54 the STAT1-independent pathway controls later viral burden and prevents DEN disease in mice.

55 Despite similar viral burden and production of the macrophage chemoattra

56 ks later, the mean values of all measures of viral burden and surrogate markers of HIV infection were

57 he viral burst leading to a reduction of the viral burden and survival of the mice.

58 ps, and persons with gaps in care had higher viral burden and transmission risk potential.

59 ere found to be strongly correlated with the viral burden and with marker genes of the IFN antiviral

60 mice, increased central nervous system (CNS) viral burdens and delayed clearance were observed.

61 1 (HIV-1) variants display exceptionally low viral burdens and do not show evidence of disease progre

62 ells which correlated with persistently high viral burdens and increased levels of CD4+ T-cell apopto

63 ) antigens had higher central nervous system viral burdens and increased mortality rates after infect

64 ibody (microMT mice) developed increased CNS viral burdens and were vulnerable to lethal infection at

65 in T cell infiltration into the CNS, reduced viral burden, and demyelination comparable to RAG1(-/-)

66 lates with lung IFN-gamma abundance, but not viral burden, and leads to enhanced susceptibility to se

67 ng Sema7A showed increased survival, reduced viral burden, and less blood-brain barrier permeability

68 o postmortem indicators of HIV encephalitis, viral burden, and presynaptic and postsynaptic neuronal

69 ion - preserved lymph node architecture, low viral burden, and viral expression were found.

70 CD4+ lymphocyte counts and lower plasma HIV viral burdens, and is not limited to those receiving pro

71 response was correlated with modulations in viral burden as assessed by detection of infectious viru

72 correlated with relative neurovirulence was viral burden as measured by both viral CA protein expres

73 regulatory T cells (Tregs) generated by high viral burden, as depletion of these cells restored SLECs

74 In the placebo group, a large viral burden at entry or delivery or a positive culture

75 lent) and Fr98/SE (slow disease) had similar viral burdens at 3 weeks postinoculation, suggesting tha

76 ain, WNV-infected CCR5-/- mice had increased viral burden but markedly reduced NK1.1+ cells, macropha

77 imary mediators of viral clearance, but high viral burden can result in deletion of antigen-specific

78 No protection, assessed by viral burdens, CD4 counts, and time to euthanasia was ob

79 er exceeded that of Fr54, reaching levels of viral burden comparable to that seen for Fr98 (rapid dis

80 excess lung damage despite similar levels of viral burden compared with lean control mice.

81 though extensive data suggest that intra-CNS viral burden correlates with both the severity of virall

82 for untargeted metagenomics correlated with viral burden determined by quantitative PCR and showed h

83 Viral burdens did not increase, and actually decreased,

84 aques, which displayed significantly reduced viral burdens during the first 18 weeks postchallenge co

85 trate ZMPSTE24-deficient mice display higher viral burdens, enhanced cytokine production, and increas

86 bjects who started the study with the higher viral burden experienced greater decreases in viral load

87 reduced early IFN-I production and augmented viral burden facilitating the expansion of natural kille

88 s, they also tolerated substantially greater viral burdens following infection.

89 immunity that, when challenged, had reduced viral burden for both influenza and RSV.

90 -seropositive subjects, all with significant viral burden (> 50,000 HIV RNA copies/mL plasma), showed

91 ected mice resulted in reduced morbidity and viral burden, improved lung compliance, and increased CD

92 te, and nonclassical monocytes) to the total viral burden in 22 human T cell leukemia virus type 1 (H

93 phonuclear neutrophil (PMN) infiltration and viral burden in brain of Opn (-/-) mice were significant

94 n animals and may play a role in controlling viral burden in established infection.

95 have been shown to inversely correlate with viral burden in HIV-1-infected individuals.

96 cessfully improved the ability to manage the viral burden in infected patients.

97 ction compared to WT animals in terms of the viral burden in infected tissues as well as elevated mor

98 from patients with PBC, suggesting a higher viral burden in lymphoid tissue.

99 on and the subsequent determination of HIV-1 viral burden in monocytes.

100 ey had more severe immunopathology, enhanced viral burden in multiple organs, and suppression of MCMV

101 virus, and this was associated with greater viral burden in multiple organs.

102 positively correlated with the magnitude of viral burden in naive and central memory CD4(+) T-cell p

103 the central nervous system (CNS) and higher viral burden in neuronal tissues.

104 The mean viral burden in persistently infected immunized macaques

105 and showed enhanced survival rate and lower viral burden in the brain after lethal WNV challenge.

106 tention in vivo in the brain correlated with viral burden in the brain and cerebrospinal fluid, and w

107 , only CCL7 deficiency resulted in increased viral burden in the brain and enhanced mortality.

108 As no difference in viral burden in the brain or spinal cord was observed af

109 +) CD8(+) T-cell trafficking, an increase in viral burden in the brain, and enhanced morbidity and mo

110 increased WNV-infected PMN infiltration and viral burden in the brain, which was coupled to increase

111 h does not influence either viral tropism or viral burden in the brain.

112 ugh this may reflect merely a higher overall viral burden in the brain.

113 enhances WNV mortality in mice and increases viral burden in the brain.

114 nd compromised T-cell mitogenesis, increased viral burden in the bursae of IBDV-infected chickens.

115 ncy of perforin molecules resulted in higher viral burden in the CNS and increased mortality after WN

116 Results indicate that SAG treatment reduced viral burden in the CNS immediately after HIV transmissi

117 High viral burden in the onset of infection drives responding

118 al lymph-node biopsies for the assessment of viral burden in these tissues.

119 itative technique was developed to determine viral burden in two important cellular compartments in l

120 ngly sensitive and precise assays to measure viral burden in various tissues and body fluids.

121 asts was associated with a downmodulation in viral burden in vivo.

122 lly reduced viral replication and infectious viral burdens in a frog kidney cell line and in tadpoles

123 nst FV3 infection, decreasing the infectious viral burdens in both cases.

124 ad (sevenfold) as well as in early set-point viral burdens in both plasma and lymphoid tissues (10-fo

125 nt to FDC may offer new avenues for reducing viral burdens in infected individuals.

126 Relatively small differences in viral burdens in peripheral tissues of TNF-R1(-/-) mice

127 High viral burdens in target tissues were associated with org

128 The viral burdens in the infected rgp120 vaccine recipients

129 Analogously, morbidity, mortality, and viral burdens in tissues were identical between Ifit1(-/

130 es in RMs and humans than in SMs; and (4) LT viral burden, including follicular dendritic cell deposi

131 High viral burden is coincident with inadequate adaptive immu

132 can be infected, but the distribution of the viral burden is differentially allocated to lymphocyte a

133 After a hamster is treated with MAb 201, its viral burden is reduced by 102.4-103.9 50% tissue-cultur

134 t CD8(+) T cell response in the face of high viral burden is vital for host survival.

135 enge markedly impaired viral replication and viral burdens, it only transiently extended tadpole surv

136 1 diversification could be related to higher viral burdens, manifestations of disease, and/or dual in

137 years viremia, a novel measure of cumulative viral burden, may provide prognostic information beyond

138 determine whether cerebrospinal fluid (CSF) viral burden measurements can assist in the evaluation o

139 ly active antiretroviral therapy in reducing viral burden, neurologic disease associated with HIV-1 i

140 e purpose of this study was to determine the viral burden of HIV-1 in the lungs by comparing HIV-1 RN

141 not correlate with the clinical severity or viral burden of secondary DV infection.

142 ere no significant differences in the tissue viral burdens or the kinetics of viral spread.

143 d lethality after WNV infection and elevated viral burden primarily in the brain, even though little

144 y-three percent of the mice with this latent viral burden reactivated in vivo following hyperthermic

145 ion of the Treg response as a result of high viral burden regulates late-stage SLEC number.

146 he hypothesis that HIV-1 infection induces a viral burden-related, global activation of the immune sy

147 Although viral burden relates to disease severity, pathogenesis i

148 ning, somewhat less so to a semiquantitative viral burden score based on numbers of HIV gp41-immunore

149 V-1 envelope protein from a donor with a low viral burden, stable CD4(+) T-lymphocyte counts, and lit

150 k of any acute toxicity or adverse effect on viral burden suggests that therapy with antiviral CTLs d

151 m, we have evaluated longitudinal changes in viral burden, T-cell subsets, and mucosal gene expressio

152 te counts were higher (P < 0.001) and plasma viral burdens tended to be lower (P = 0.08) in HIV-infec

153 at received adjuvanted vaccines showed lower viral burden than the control or unadjuvanted vaccine gr

154 ptible to WNV infection and develop a higher viral burden than wild-type (WT) mice.

155 l confronts the immune system with a chronic viral burden that may involve immune cells themselves an

156 s a less expensive alternative for measuring viral burden that quantifies RT enzyme activity in clini

157 ing infection of Ctx(-) mice, while they had viral burdens that were identical to those of WT animals

158 HIV-1 RNA levels in plasma may influence CSF viral burden, these variables were examined as potential

159 IFNalpha therapy is associated with reduced viral burden, this cytokine also mediates immune dysfunc

160 RP v1.7 did not detect HAdV with either low viral burden (threshold cycle values of >30) or nonrespi

161 ts who are infected with HCV by reducing the viral burden through specific targeting and cleavage of

162 se activity, but also leads to increased HCV viral burden via alterations in immunologic viral survei

163 Although no difference in viral burden was detected in peripheral tissues, greater

164 more vulnerable to lethal WNV infection, the viral burden was greater only within the CNS, particular

165 N-alpha/betagammaR(-/-) mice even though the viral burden was heavy.

166 The BAL viral burden was higher than plasma HIV-1 in tuberculosi

167 During peak loss of CD4+ cells, high viral burden was observed, suggesting that loss of CD4+

168 Viral burden was quantified by a microculture technique

169 serum markers of immunologic activation, and viral burden were assessed in 75 human immunodeficiency

170 Levels of viral burden were compared across risk group and gender

171 iring high concentrations of Ag for reducing viral burden when adoptively transferred into SCID mice.

172 e P receptor expression, showed an increased viral burden when compared with syngeneic C57BL/6 mice.

173 ansfer of ZIKV-immune CD8(+) T cells reduced viral burdens, whereas their depletion led to higher tis

174 ypes in Nigeria exhibit long periods of high viral burden, which can contribute to increased transmis

175 High viral burden with EBV was associated with the developmen

176 on of macrophages and T cells to the overall viral burden within lymphoid tissue.

177 ) resulted in increased survival and reduced viral burden within the brain and liver compared to thos

178 ty that correlated with a >3 log increase in viral burden within the brains as compared with control

179 mice, an infection model that exhibits high viral burden within the central nervous system.