ライフサイエンスコーパス: secondary infection

1 orting an ability to distinguish primary and secondary infections).

2 sly infected animals were not colonized upon secondary infection.

3 CD8+ T cells and recall responses following secondary infection.

4 T cells were virtually unable to expand upon secondary infection.

5 lizing MAbs against the four serotypes after secondary infection.

6 way, increasing the lung's susceptibility to secondary infection.

7 ble to proliferate or produce cytokines upon secondary infection.

8 e patients, with higher overall clonality in secondary infection.

9 ion of the memory CD8 T cell response during secondary infection.

10 Responses were less robust after secondary infection.

11 matically different responses to primary and secondary infection.

12 ons in CD4 T cell IFN-gamma production after secondary infection.

13 ected and B cell-deficient mice succumbed to secondary infection.

14 d Salmonella and examined protection against secondary infection.

15 ctor cytokines or proliferate in response to secondary infection.

16 s years or even decades following primary or secondary infection.

17 ollowing a primary infection that prevents a secondary infection.

18 O56 has a superior CD4(+) recall response to secondary infection.

19 sufficient to promote a deadly S. pneumoniae secondary infection.

20 nti-TSLP were administered during primary or secondary infection.

21 es, their distribution revealed instances of secondary infection.

22 e and adaptive responses to both primary and secondary infection.

23 for virus neutralization and defense against secondary infection.

24 tomatic HIV and decreased in HIV wasting and secondary infection.

25 t correlates specifically with a subclinical secondary infection.

26 8 T cell precursor frequency) present during secondary infection.

27 individuals experiencing primary instead of secondary infection.

28 ter longevity and proliferative responses to secondary infection.

29 ost TCEs examined are poorly responsive to a secondary infection.

30 orrelated with reduced early protection from secondary infection.

31 al septic insult increases susceptibility to secondary infection.

32 esponses may lead to enhanced disease during secondary infection.

33 nflammation was no longer significant during secondary infection.

34 frequencies of mutations among patients with secondary infection.

35 c treatment and did not confer protection to secondary infection.

36 tured into memory T cells able to respond to secondary infection.

37 that were capable of mediating immunity to a secondary infection.

38 ng primary infection; NP366 dominates during secondary infection.

39 er the immune response during a heterologous secondary infection.

40 mory T cells responded preferentially to the secondary infection.

41 at are capable of responding rapidly after a secondary infection.

42 quent episodes of lytic viral replication or secondary infection.

43 aster viral clearance were observed during a secondary infection.

44 the relative strength of initial primary to secondary infection.

45 atum was necessary for control of primary or secondary infection.

46 idly and upregulated IL-10 expression during secondary infection.

47 prevent nonessential immune responses during secondary infection.

48 deficiency is no longer evident following a secondary infection.

49 6-374/Db-specific CD8+ memory T cells during secondary infection.

50 tent with immune suppression at the onset of secondary infection.

51 hance the proliferation of antibodies during secondary infection.

52 the adaptive immune response to primary and secondary infection.

53 nduced in serum with anamnestic responses to secondary infection.

54 ow with no anamnestic responses in mice with secondary infection.

55 ytes capable of mounting a rapid response to secondary infection.

56 ession of these molecules was observed after secondary infection.

57 roductive type-2 immunity during primary and secondary infection.

58 trafficking and function during primary and secondary infection.

59 led to proliferate during the early phase of secondary infection.

60 ced by plasmablasts a few days after natural secondary infection.

61 effects of IFN-alpha are prevented during a secondary infection.

62 did not affect T cell recall responses upon secondary infection.

63 clears adult worms or controls fecundity in secondary infection.

64 irment similar to those of mice experiencing secondary infection.

65 red lung TCD8s, similar to mice experiencing secondary infection.

66 and displayed diminished recall responses on secondary infection.

67 engendering myeloid cells that fail to clear secondary infection.

68 ta show that eosinophils protect the host in secondary infection.

69 enhance infection with other serotypes in a secondary infection.

70 ction or during reactivation from latency or secondary infection.

71 U admission than those who did not develop a secondary infection.

72 donor skin sites, and organs susceptible to secondary infection.

73 ls and monocytes and contributed to limiting secondary infection.

74 laboratory-confirmed influenza, to identify secondary infections.

75 mmunity, confers nonspecific protection from secondary infections.

76 ation is thought to influence the outcome of secondary infections.

77 s associated with longer hospitalization and secondary infections.

78 nd 64% for DENV-4, compared with primary and secondary infections.

79 tent immunosuppression and susceptibility to secondary infections.

80 nosuppression that favors the development of secondary infections.

81 ral organs and contributes to the control of secondary infections.

82 on associated with it, as well as to prevent secondary infections.

83 y infection and protects distal tissues from secondary infections.

84 in the kinetic profiles between primary and secondary infections.

85 associated with increased susceptibility to secondary infections.

86 thogen-specific, increased susceptibility to secondary infections.

87 RATIONALE: Sepsis can be complicated by secondary infections.

88 protective immunity and disease severity in secondary infections.

89 likely responsible for initiating bloodborne secondary infections.

90 nucleoli were found to retain infectivity in secondary infections.

91 pism and pathogenesis of DENV in primary and secondary infections.

92 pet hamsters, mice, or rats, and 2 (9%) had secondary infections.

93 ributes to accelerated immune control during secondary infections.

94 d within 4 weeks, with faster clearance upon secondary infections.

95 y a key role in cellular immune responses to secondary infections.

96 y CD8 T cells which most effectively control secondary infections.

97 hs a year in developing countries because of secondary infections.

98 es can vary dramatically between primary and secondary infections.

99 pt transmission and the resultant cascade of secondary infections.

100 with a greater propensity for opportunistic secondary infections.

101 e of an epidemic outbreak, and the number of secondary infections.

102 f enhanced DENV infection and disease during secondary infections.

103 may increase an organism's susceptibility to secondary infections.

104 manifested as an increased susceptibility to secondary infections.

105 al fate of macrophages and susceptibility to secondary infections.

106 ent serotypes and of subsequent heterologous secondary infections.

107 ly develop either subclinical or symptomatic secondary infection 6-11 months after the baseline blood

108 tisone vs placebo groups, 21.5% vs 16.9% had secondary infections, 8.6% vs 8.5% had weaning failure,

109 After vaccination, or during secondary infection, adaptive immune responses can enhan

110 ts into the mechanisms for graft failure and secondary infection after burn injury.

111 and community acquired pneumonia and causes secondary infection after influenza A.

112 Pneumonia occurring as a secondary infection after influenza is a major cause of

113 During secondary infections, Ag-specific memory Tregs showed ac

114 n regarding any potential immune barriers to secondary infection also currently is unavailable.

115 or susceptible contacts elevated the odds of secondary infection among susceptible contacts: The pres

116 suppressed status that increases the risk of secondary infection and death.

117 nce, we sought to ascertain the incidence of secondary infection and genetic variability in populatio

118 Secondary infection and higher viremia were independent

119 model of sepsis, we show that tolerance to a secondary infection and its associated mortality were ef

120 plosive, peaking at approximately 12 h after secondary infection and terminating hours thereafter.

121 s-induced alterations in the control of this secondary infection and the associated naive Ag-specific

122 ell to encounter the virus after primary and secondary infection and thus the consequences of their i

123 ficiently, it may increase susceptibility to secondary infections and alter innate immune responses t

124 theless causes other side-effects, including secondary infections and cancer.

125 oups of dengue viruses, and the link between secondary infections and DENV disease pathogenesis, has

126 also proves useful for inferring numbers of secondary infections and identifying heterogeneous infec

127 ering critically ill patients susceptible to secondary infections and increased mortality.

128 oparalysis may render patients vulnerable to secondary infections and is associated with impaired out

129 itis C virus (HCV) infection rapidly control secondary infections and reduce the risk of virus persis

130 injury, response to treatment, prevention of secondary infection, and control of glaucoma.

131 ss inflammation at the site of a primary and secondary infection, and exhibited an impaired delayed-t

132 xpanded similarly to wild-type T cells after secondary infection, and immunized IL-7Ralpha transgenic

133 tory response may lead to immunosuppression, secondary infection, and late deaths.

134 a potential risk of delaying wound healing, secondary infections, and cancer.

135 ortality from sepsis frequently results from secondary infections, and the extent to which sepsis aff

136 HIV wasting and secondary infections are also associated with increased

137 gue hemorrhagic fever (DHF), the majority of secondary infections are subclinical or mild.

138 ematical models assume that all heterologous secondary infections are subject to enhanced susceptibil

139 ease, which suggests that only a minority of secondary infections are subject to enhancement.

140 eed one, where R(0) is the average number of secondary infections arising from one infected individua

141 it provided equivalent protection against a secondary infection as observed in WT mice.

142 assessed using prevention of influenza, not secondary infections, as an endpoint.

143 ting from a traumatic injury and followed by secondary infection at the site.

144 rity; duration of symptoms; or prevalence of secondary infection between the 2 groups.

145 ocked attachment, whereas those derived from secondary infection blocked DENV postattachment.

146 tes the RSV-specific CD8+ T cell response to secondary infection but does not independently regulate

147 icates that T(CM) cells may not only control secondary infections, but may also contribute to the con

148 immunopathogenesis of dengue disease during secondary infection by a heterologous serotype.

149 ondary infection by the ELISPOT assay and in secondary infection by MHC/peptide tetramer staining.

150 ablished virus infection to interfere with a secondary infection by related viruses.

151 ios were observed consistently in primary or secondary infection by the ELISPOT assay and in secondar

152 ablished virus infection to interfere with a secondary infection by the same or a closely related vir

153 id not interfere with the establishment of a secondary infection by the same virus labeled with a dif

154 ithelial submucosa of mice after primary and secondary infections by a natural gastrointestinal paras

155 ion is a widespread phenomenon that prevents secondary infections by closely related viruses.

156 rement of these cells for mCTL recall during secondary infections by different pathogens.

157 These cells were susceptible to secondary infections by HSV-1.

158 for transmission between macrophages, since secondary infections by relA spoT mutants were restored

159 e chemokine-binding activity is mitigated in secondary infections by the production of anti-gG antibo

160 Thus, this work highlights the impact a secondary infection can have on leishmaniasis and demons

161 was estimated to be such that the number of secondary infections caused by resistant strains is only

162 A-primed animals were less protected against secondary infection compared with those primed with LPS.

163 ased from 23% to 45% (Ptrend < .0001), while secondary infections decreased from 45% to 26% (Ptrend =

164 n wild-type mice following either primary or secondary infection despite the obvious deficits in adap

165 th primary infection died, whereas none with secondary infection did.

166 after HSCT (eg, graft-versus-host disease or secondary infections) did not differ between groups.

167 of memory CD8+ T cells that replicate during secondary infections differ over whether such cells had

168 ADCC activity in plasma obtained before secondary infection directly correlated with neutralizin

169 8 T cell populations that were induced after secondary infection displayed polyfunctionality and were

170 ponses to mycobacteria and impair control of secondary infections distal to the gut.

171 ty of a primary challenge to protect against secondary infection (e.g., during vaccination) independe

172 virus was far more virulent and established secondary infection earlier than AcLate21/20-64HB, but w

173 udies, we have demonstrated both primary and secondary infections, expanded tissue tropism, and exten

174 es and artificially limiting the duration of secondary infection following heterologous rechallenge a

175 The average number of secondary infections generated throughout the entire inf

176 circulating in enormous numbers during acute secondary infection have not been studied.

177 Enhanced secondary infections have been implicated in the majorit

178 .21, 0.42; P < 0.001) and by 59% following a secondary infection (hazard ratio = 0.41, 95% confidence

179 for the differentiation between primary and secondary infections, hence, facilitating epidemiologica

180 used response contribute to the clearance of secondary infections; however, a more diverse pool of an

181 lates with reduced likelihood of symptomatic secondary infection in a longitudinal pediatric dengue c

182 lung and bladder, which are common sites of secondary infection in burn-injured patients.

183 RM, or for the establishment of a persistent secondary infection in CMV-infected RM transiently deple

184 increased mortality to trauma combined with secondary infection in the aged are not due to an exagge

185 to vector, thereby abrogating the cascade of secondary infections in humans.

186 luenza A virus in B6 mice during primary and secondary infections in vivo.

187 role of poorly understood processes such as secondary infections, in population-level dynamics of di

188 c receptor-bearing cells during a subsequent secondary infection, increasing viral replication and th

189 serotypes of dengue virus and, furthermore, secondary infection is a major risk factor in dengue hem

190 Thus, chlamydial disease after secondary infection is a temporal dysregulation of the T

191 uggest that the increased risk of DHF during secondary infection is due to immunopathology partially

192 ework in which the population susceptible to secondary infection is split into a group prone to enhan

193 nfection remains poorly understood, although secondary infection is strongly associated with more sev

194 ypothesis for the increased severity seen in secondary infections is antibody-dependent enhancement (

195 The development of these secondary infections is due to bacterial dissemination f

196 Variation in the number of secondary infections is extremely difficult to estimate

197 that T. viride can control primary, but not secondary, infection is robust to inclusion of the laten

198 empirical data show that only a minority of secondary infections lead to severe disease, which sugge

199 T triggering can be blocked by secondary infections, leading to the state of lysis inhi

200 er to persistent, recurrent, nosocomial, and secondary infections, many investigators have turned the

201 nts are connected by networks of primary and secondary infection mechanisms.

202 Among secondary infections, median titers in serum were 2072 (

203 IL-10(-/-) mice cleared primary and secondary infection more rapidly than wild-type controls

204 esumably lead to increased susceptibility to secondary infections, multiorgan failure, and death.

205 ve against dengue hemorrhagic fever (DHF) in secondary infections (odds ratio [OR] = 0.46, 95% confid

206 In contrast, secondary infection of H1N1 preimmune ferrets with an an

207 sinophil ablation had a pronounced effect on secondary infection of skeletal muscle by migratory newb

208 Analysis of bacterial growth after a secondary infection of systemic leaves revealed that the

209 In LIN, secondary infection of T4-infected cells results in a dr

210 The effect of secondary infections on CD4 T-cell-regulated chronic gra

211 Because each may increase following secondary infection or mutator emergence, we sought to a

212 ithelium may increase the risk for acquiring secondary infections or allergen sensitization.

213 viruses we estimate that the mean number of secondary infections per infected farm is greater than o

214 ng the TB transmission rate (i.e., number of secondary infections per infectious case) in the hotspot

215 people aim to maintain the average number of secondary infections per infectious person at one or les

216 ations, we projected the expected numbers of secondary infections per infectious person for measles,

217 D8+ T cell responses during both primary and secondary infection, perhaps accounting for the incomple

218 Secondary infection predisposes individuals to more seve

219 to discriminate individuals with primary and secondary infection presenting as dengue fever (DF; mild

220 disease that represent the average number of secondary infections produced by a random infectious ind

221 IgE(-/-) cohorts subjected to a secondary-infection protocol were able to clear the chal

222 IgE(-/-) mice were subjected to primary- and secondary-infection protocols.

223 t the analyses on the balance of primary and secondary infection provide the epidemiologist with some

224 ion of the immune response after primary and secondary infections provide new insights into HLA-restr

225 The model represents primary and secondary infection rates and a time-varying host suscep

226 Adverse events, including secondary infection rates, did not differ between study

227 During secondary infection, rats expel 90-99% of T. spiralis fi

228 d CD4(+) T cell responses during primary and secondary infections, respectively.

229 o retain and present antigen in a subsequent secondary infection, resulting in diminished B cell resp

230 entry into Fc receptor bearing cells during secondary infection, resulting in enhanced viral replica

231 ers in patients who later went on to develop secondary infections revealed a more dysregulated host r

232 Patients who developed a secondary infection showed higher disease severity score

233 /-)M3(-/-) CD8(+) T cells do not expand upon secondary infection, similar to what has been observed f

234 ccording to their disease phase, primary and secondary infection status, and disease severity, measur

235 teremia, which frequently results in serious secondary infections such as infective endocarditis, ost

236 n regarding possible coinfections or induced secondary infections, such as virally induced bacterial

237 However, in the case of secondary infections, such MBC-based approaches fail to

238 ivation of memory B cells early during acute secondary infection, suggesting reactivation from a prev

239 at of wild-type mice during both primary and secondary infection, suggesting that CD28-mediated costi

240 prolonged infection course after primary or secondary infection, suggesting that CD40-CD40L costimul

241 ite phenology altered host susceptibility to secondary infections, symbiont interactions and ultimate

242 e robust help for CD8(+) T-cell responses to secondary infection than LLO56.

243 CD8 T cells and were less protected against secondary infection than were wild-type mice.

244 idity and mortality, usually associated with secondary infections that have a predilection to the res

245 When memory Tregs were depleted before secondary infection, the magnitude of the Ag-specific me

246 Within 6 h following secondary infection, the production of gamma interferon

247 Upon secondary infection, these central memory T cells become

248 ly asymmetric, increased transmissibility of secondary infections through immune enhancement increase

249 ntially reduced proliferative expansion upon secondary infection using multiple challenge models.

250 Assuming each primary infection causes 1.5 secondary infections, vaccinating 40% of the population

251 On secondary infection, virus-specific CD8+ T cells that be

252 d parasite control in WSX-1(-/-) mice during secondary infection was associated with elevated systemi

253 The acute response after heterologous secondary infections was enhanced compared with the acut

254 After secondary infection, we observed substantial increases i

255 lls are strictly required for the control of secondary infection, we observed that only TCR-beta defi

256 odies cloned from patients with heterologous secondary infection, we tested the protective value of t

257 , survival up to 180 days, and assessment of secondary infections, weaning failure, muscle weakness,

258 ls and the associated rapid clearance of the secondary infection were not affected by treatment with

259 unctional attributes and expansion after the secondary infection were not improved.

260 weakly neutralizing MAbs, whereas those from secondary infection were primarily GR, high-avidity, and

261 eas most E-specific B cells in patients with secondary infection were serotype-cross-reactive and sec

262 Excluding SSEs, we estimate that 2.7 secondary infections were generated per case on average

263 nce patterns that shifted over time or after secondary infection, whereas vaccine-generated immunodom

264 ility that patients with sepsis developing a secondary infection while in the intensive care unit (IC

265 with active underlying rheumatic disease and secondary infection who are being treated with immunosup

266 ontribute to increased disease severity upon secondary infection with a different DENV serotype.

267 immunity against the infecting serotype, but secondary infection with a different serotype carries a

268 serotype causes less effective response upon secondary infection with a different serotype, predispos

269 During secondary infection with a heterologous dengue virus (DE

270 risk factor for developing severe dengue is secondary infection with a heterologous serotype.

271 level of virus replication seen during both secondary infection with a heterotypic virus and during

272 eutralize DENV but also enhance disease upon secondary infection with another DENV serotype.

273 ble to mount an effective memory response to secondary infection with BCG.

274 the respiratory epithelium that facilitates secondary infection with common bacterial pneumopathogen

275 nocompetent individuals to severe illness on secondary infection with H. influenzae by a mechanism th

276 ectrum of the host memory response against a secondary infection with H. polygyrus bakeri was severel

277 tion that are similar to those observed in a secondary infection with Heligmosomoides polygyrus.

278 ase is frequently observed in the setting of secondary infection with heterologous dengue virus serot

279 all response required for protection against secondary infection with L. monocytogenes.

280 Abs confer protection from secondary infection with Legionella pneumophila, the cau

281 layed an increase in skin parasite load upon secondary infection with Leishmania major as well as a r

282 robust and rapidly fatal immune responses to secondary infection with lymphocytic choriomeningitis vi

283 in the lungs of cotton rats after primary or secondary infection with respiratory syncytial virus (RS

284 dies have correlated immune responses during secondary infection with severity of disease, to our kno

285 for each comparison) as was the presence of secondary infection with Staphylococcus aureus (p = 0.00

286 ed to address the function of eosinophils in secondary infection with T. spiralis.

287 infection were found to expand earlier after secondary infection with the pandemic H1N1 virus than CD

288 ich a preexisting viral infection prevents a secondary infection with the same or a closely related v

289 n which a primary viral infection prevents a secondary infection with the same or closely related vir

290 es during primary and at the early stages of secondary infection with WN virus.

291 We thus investigated the response to secondary infections with an engineered, but still highl

292 sion, leading to increased susceptibility to secondary infections with associated late mortality.

293 est in the field of dengue viruses, in which secondary infections with different DENV serotypes incre

294 been implicated in the immunopathogenesis of secondary infections with heterologous DENV serotypes, t

295 red how XCR1(+) DCs promote mCTL recall upon secondary infections with Listeria.

296 ry infection and their propensity to develop secondary infections with pathogens that are often not p

297 e septic patients are highly susceptible to "secondary" infections with intracellular pathogens that

298 ion among household contacts and the risk of secondary infection within households using an individua

299 Influenza and pneumococcal vaccines reduce secondary infections within the lungs; however, their ef

300 on can dramatically influence the outcome of secondary infections, yet little is known about the dete