ライフサイエンスコーパス: virus clearance

1 e with BR/08, but did not result in complete virus clearance.

2 t explain its negative effect on hepatitis C virus clearance.

3 iorates clinical disease without diminishing virus clearance.

4 kidneys from day 6 onward, in parallel with virus clearance.

5 nhanced oligodendroglial tropism and delayed virus clearance.

6 fect virus distribution and actually delayed virus clearance.

7 cted B-cell-deficient mice following initial virus clearance.

8 to inhibit virus production and elicit early virus clearance.

9 spite similar lung virus titers and rates of virus clearance.

10 al), although GKO mice exhibited a defect in virus clearance.

11 nd examined whether T cells were involved in virus clearance.

12 of nonimmunized mice, indicating accelerated virus clearance.

13 ly virus replication but is not required for virus clearance.

14 ersistence in macrophages and interfere with virus clearance.

15 d to favor cytokine secretion as the mode of virus clearance.

16 mechanisms were involved in the MAb-mediated virus clearance.

17 and, possibly, good interferon response and virus clearance.

18 esulted in an extremely significant delay in virus clearance.

19 ng IFN-I receptor (IFNAR) signaling promotes virus clearance.

20 ave been associated with reduced hepatitis C virus clearance.

21 ramatically impaired CD8(+)-T-cell-dependent virus clearance.

22 nflammatory signaling that can persist after virus clearance.

23 improves T cell functionality and increases virus clearance.

24 whereas the T-cell response was required for virus clearance.

25 w to high pathogenicity, as well as impeding virus clearance.

26 from lethal disease and effected more-rapid virus clearance.

27 innate and adaptive immune responses mediate virus clearance.

28 pontaneous and treatment-induced hepatitis C virus clearance.

29 specific immunity while preventing premature virus clearance.

30 trum of genes activated during noncytopathic virus clearance.

31 mild enhancement of replication and delayed virus clearance.

32 ells results in almost complete Epstein-Barr virus clearance.

33 and organ function at the cost of prolonging virus clearance.

34 pavir was safe and significantly accelerated virus clearance.

35 obust adaptive immune responses resulting in virus clearance.

36 ically affect weight loss and survival after virus clearance.

37 CD8(+) effectors and ultimately compromises virus clearance.

38 fection and, more recently, with accelerated virus clearance.

39 cause immunosuppressive effects that impede virus clearance.

40 D8(+) T cell effector functions critical for virus clearance.

41 gene expression, leading to inflammation and virus clearance.

42 during viremia and even several months after virus clearance.

43 at stimulate T cell proliferation well after virus clearance.

44 tivity, influenza-specific IgG response, and virus clearance.

45 inhibition titers, CTL activity, and earlier virus clearance after homologous and heterosubtypic [A/P

46 The effector responsible for virus clearance also mediated illness, suggesting that e

47 n, gradually returning to the baseline after virus clearance, although the IL-22 gene expression was

48 ted animals exhibited an accelerated rate of virus clearance, an accelerated appearance of higher inf

49 y reaction in the cornea which leads to both virus clearance and chronic lesions that are orchestrate

50 persist in draining lymph nodes (DLNs) after virus clearance and could, therefore, affect the adaptiv

51 ese data support a role of CD4(+) T cells in virus clearance and demyelination.

52 on of normally resistant B10 mice results in virus clearance and development of inflammatory demyelin

53 n the airways served to accelerate influenza virus clearance and enhance infection recovery.

54 Our results show that type I IFNs facilitate virus clearance and enhance the migration and maturation

55 vaccination resulted in more efficient lung virus clearance and enhanced cellular recall responses a

56 ll immune responses, which are important for virus clearance and for protection against myelin destru

57 he model illustrates how the balance between virus clearance and immune exhaustion may be disrupted w

58 flamed musculoskeletal tissues that inhibits virus clearance and impedes disease resolution in an arg

59 luenza virus-specific CD8 T cells to promote virus clearance and improve the outcome of infection.

60 ammation in these animals results in greater virus clearance and improved survival.

61 y virus infections plays a prominent role in virus clearance and is essential for resistance to reinf

62 Respiratory syncytial virus clearance and levels of Th1 effector cytokine IFN-

63 Accelerated virus clearance and limited spread in immunized mice was

64 antiviral contributions of CD4(+) T cells in virus clearance and pathology, memory CD4(+) T cells pur

65 Thus, IRF-3 serves to facilitate virus clearance and prevent tissue injury in response to

66 A (miR) patterns associated with spontaneous virus clearance and recovery (CVB3-ELIM) versus virus pe

67 R-P1B, but not Clr-b, results in accelerated virus clearance and recovery from MCMV infection.

68 n of CD4+ and CD8+ effector T lymphocytes in virus clearance and recovery, we have examined the host

69 sponses in neonates that result in increased virus clearance and reduced lung pathology postchallenge

70 ll-mediated immunity that persists following virus clearance and results in secondary infections.

71 other Ig classes show significantly reduced virus clearance and survival rates compared with wild-ty

72 parenchymal penetration of T lymphocytes for virus clearance and survival, suggesting that perivascul

73 This suppression leads to incomplete virus clearance and the establishment of virus persisten

74 sistent virus infection resulted in enhanced virus clearance and was CD4 T cell-dependent.

75 dues S510 to 518 (S510), resulted in delayed virus clearance and/or virus persistence we selected iso

76 requency, NO levels in lung lavage, rates of virus clearance, and anti-RSV Ab titers were determined.

77 body to the E2 glycoprotein is important for virus clearance, and B cells enter the CNS along with CD

78 CD8(+) T cells to the infected lung, delayed virus clearance, and increased morbidity.

79 esulted in a robust T cell response, earlier virus clearance, and increased survival.

80 expression of TNF-alpha and NO, accelerates virus clearance, and increases the anti-F and anti-G Ab

81 such as hypoxia, multiple organ dysfunction, virus clearance, and shortened liberation of ventilator

82 ne responses that may be responsible for the virus clearance, and should serve as a benchmark for SAR

83 ction of the innate immune responses to IAV, virus clearance, and the development of pulmonary injury

84 virus replication in the eye, the most rapid virus clearance, and the lowest level of explant reactiv

85 During virus clearance antiviral cytokines are thought to block

86 al T cell responses that lead to accelerated virus clearance, approximating what occurs during attenu

87 ce of virulence and immune response mediated virus clearance are also found to influence the fitness

88 l capacities of CD8(+) T cells important for virus clearance are influenced by interactions with anti

89 tion of CD8 T cells, the effectors of rabies virus clearance are more commonly targeted to the cerebe

90 lization of memory T cells to the DLNs after virus clearance as a consequence of presentation of resi

91 emonstrated that T cells are responsible for virus clearance, as intravenous adoptive transfer of SAR

92 ined on the VLP diet to the AP diet improved virus clearance, as well as protective immunity to viral

93 to irradiated C57BL/6 mice resulted in rapid virus clearance, but clearance was greatly delayed in re

94 Neutralization of IL-17 augments virus clearance by eliminating virus-infected cells and

95 cause to an infection characterized by rapid virus clearance by innate and adaptive immune system com

96 nomes into siRNAs of discrete sizes to guide virus clearance by RNA interference.

97 and encephalitis, followed by host death or virus clearance by the immune system.

98 trolled, at least in the initial weeks after virus clearance, by residual antigen in the lung-drainin

99 th brains and spinal cords following initial virus clearance coincided with an overall progressive lo

100 ired interleukin-12 expression, and impaired virus clearance compared to mice expressing TLR4.

101 nstitutively overexpress IL-4 showed delayed virus clearance compared with mice of the FVB/N control

102 ction of Adamts5-/- mice resulted in delayed virus clearance, compromised T cell migration and immuni

103 gs prior to RSV infection results in delayed virus clearance concomitant with an early lag in the rec

104 iated illness, suggesting that efficiency of virus clearance determined disease expression.

105 observed to mediate partial (but incomplete) virus clearance during acute LCMV infection as compared

106 d with better antibody responses, more-rapid virus clearance, fewer Th17 cells, and more-potent regul

107 Virus clearance followed similar kinetics in all mice, c

108 nt replication in cultured cells and delayed virus clearance from ferret respiratory organs for Norwa

109 usly into NS5A-Tg mice and control mice, and virus clearance from liver was compared over a time cour

110 neurons and the molecular events involved in virus clearance from mature neurons.

111 ansfer of memory cells from B+/+ mice led to virus clearance from persistently infected B+/+ recipien

112 that class II gene products are required for virus clearance from the CNS but not for demyelination a

113 tudied the development of clinical signs and virus clearance from the CNS in knockout mice lacking ei

114 NS infections, we investigated mechanisms of virus clearance from the CNS of neonatal BALB/c mice inf

115 nodominant S510 epitope is not essential for virus clearance from the CNS, the S510 inactivating muta

116 None of the vaccines resulted in improved virus clearance from the inoculation site, and none sign

117 owever, splenectomy did not seriously impede virus clearance from the lung and, despite a substantial

118 genitors in the bone marrow and also limited virus clearance from the lung.

119 une mice and a more pronounced diminution of virus clearance from the vaginal mucosa despite the pres

120 Although a delay in the kinetics of virus clearance has been demonstrated in previous studie

121 ination of macrophage subpopulations impeded virus clearance, impaired the generation of class I MHC-

122 mportant role of CMI in favoring hepatitis C virus clearance in CC patients.

123 ic T-lymphocyte (CTL) recognition and impede virus clearance in infected hosts.

124 anti-NP IgG specifically promoted influenza virus clearance in mice by using a mechanism involving b

125 inetics of the T cell response and influenza virus clearance in mice vaccinated with the NP or PA pep

126 n, while IL-1 may be important for effective virus clearance in nonlethal H5N1 disease.

127 ted in the presence of IL-4 in comparison to virus clearance in recipients of cells stimulated in the

128 polyhedrovirus (BmNPV) genome DNA to promote virus clearance in silkworms.

129 ) in Drosophila, which is capable of a rapid virus clearance in the absence of expression of a virus-

130 This immunity system is capable of rapid virus clearance in the absence of FHV B2 protein, which

131 ell entry across the blood-brain barrier and virus clearance in the absence of overt sequelae.

132 We analyzed the rate of virus clearance in the general circulation in rhesus mac

133 ll phenotype correlates with a lower rate of virus clearance in the severe infection and is partially

134 henotype as the critical factors involved in virus clearance in this model.

135 8 T cells, the primary adaptive mediators of virus clearance in wt mice.

136 t their possible role as direct mediators of virus clearance is less well characterized.

137 ilure since infected myocytes are sparse and virus clearance is rapid.

138 Virus clearance is slightly delayed following depletion

139 ing the pivotal role of CTLs and antibody in virus clearance, it is reasonable to assume a redundancy

140 Concomitant with ineffective virus clearance, macrophage numbers were increased in th

141 evaluated for changes in neuroinflammation, virus clearance, neuropathology, and development of brai

142 lls at physiological levels neither enhanced virus clearance nor altered clinical progression.

143 tricted CD8+ CTL response and contributed to virus clearance not involving cytolytic mechanisms.

144 Virus clearance occurred in three phases: clearance of i

145 xtensive inflammatory-cell infiltration with virus clearance occurring 6-8 d after infection.

146 mias were similar for both R5- and X4-tropic viruses, clearance of scSIV(mac)155T3 TM(stop) was signi

147 the pathogenesis of CNS inflammation, during virus clearance ONOO(-) is produced without pathological

148 Quantitative analysis of Sindbis virus clearance over 6 months shows three phases: day 5-

149 minants of hepatitis B virus and hepatitis C virus clearance, persistence, and virus-induced liver di

150 Phase 1/2 declines, free virus clearance rate, and infected hepatocyte death rate

151 To determine whether virus clearance requires both activities, we measured th

152 of CD8(+) cytotoxic T lymphocytes in measles virus clearance, rhesus monkeys were depleted of CD8(+)

153 Concomitant with virus clearance, survivors mounted a robust Ebola-virus-

154 evels of type I interferon (IFN), and slower virus clearance than did Bc mice.

155 rus-neutralizing Ab may be more important in virus clearance than the infiltration of circulating Ab.

156 une response may contribute less than 20% to virus clearance-the rest is taken care of by the stochas

157 o a Th1 response that was able to facilitate virus clearance upon heterosubtypic virus challenge.

158 Interestingly, although virus clearance was delayed, lack of the virus-specific

159 also suppressed by talampanel treatment, and virus clearance was delayed.

160 Early virus clearance was demonstrated in radiation chimeras i

161 Partial virus clearance was dependent on CD8(+) cells.

162 In both models of CD4+ T-cell deficiency, virus clearance was incomplete and persisted at low leve

163 As expected, TKO virus clearance was significantly delayed in Ab-deficien

164 Congruent with virus clearance was the recruitment of CD8(+) T cells in

165 of the inflammatory response associated with virus clearance, we reasoned that decreasing the amount

166 pression of virus replication and subsequent virus clearance were necessary for preventing CTL escape

167 G protein-specific CD4 T cell responses, and virus clearance were not altered in IL-13-deficient mice

168 aive cells before infection, the kinetics of virus clearance were similar in all three mouse strains,

169 when used in prophylaxis and effected rapid virus clearance when used as treatment.

170 APC-CD8 pathway is needed in order to ensure virus clearance when virus load is reduced by the immune

171 n asymptomatic and apathogenic infection and virus clearance, while high-dose (10(6) TCID(50)) inocul

172 factors, which are critical in orchestrating virus clearance without the development of cytopathic ef