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 led to proliferate during the early phase of secondary infection.

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

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

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

6 clears adult worms or controls fecundity in secondary infection.

7 irment similar to those of mice experiencing secondary infection.

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

9 and displayed diminished recall responses on secondary infection.

10 engendering myeloid cells that fail to clear secondary infection.

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

12 enhance infection with other serotypes in a secondary infection.

13 ction or during reactivation from latency or secondary infection.

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

15 ls and monocytes and contributed to limiting secondary infection.

16 sly infected animals were not colonized upon secondary infection.

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

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

19 lizing MAbs against the four serotypes after secondary infection.

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

21 ble to proliferate or produce cytokines upon secondary infection.

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

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

24 Responses were less robust after secondary infection.

25 matically different responses to primary and secondary infection.

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

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

28 d Salmonella and examined protection against secondary infection.

29 ctor cytokines or proliferate in response to secondary infection.

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

31 ollowing a primary infection that prevents a secondary infection.

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

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

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

35 es, their distribution revealed instances of secondary infection.

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

37 for virus neutralization and defense against secondary infection.

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

39 t correlates specifically with a subclinical secondary infection.

40 8 T cell precursor frequency) present during secondary infection.

41 individuals experiencing primary instead of secondary infection.

42 ter longevity and proliferative responses to secondary infection.

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

44 orrelated with reduced early protection from secondary infection.

45 al septic insult increases susceptibility to secondary infection.

46 esponses may lead to enhanced disease during secondary infection.

47 nflammation was no longer significant during secondary infection.

48 frequencies of mutations among patients with secondary infection.

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

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

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

52 ng primary infection; NP366 dominates during secondary infection.

53 er the immune response during a heterologous secondary infection.

54 mory T cells responded preferentially to the secondary infection.

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

56 quent episodes of lytic viral replication or secondary infection.

57 generate a more rapid and robust response to secondary infection.

58 iled to mount an improved recall response to secondary infection.

59 tion and maintenance and reduced response to secondary infection.

60 e important for sterilizing immunity against secondary infection.

61 acterial killing and improved healing upon a secondary infection.

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

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

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

65 uring sepsis decreased the susceptibility to secondary infection.

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

67 trafficking and function during primary and secondary infection.

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

69 f enhanced DENV infection and disease during secondary infections.

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

71 manifested as an increased susceptibility to secondary infections.

72 al fate of macrophages and susceptibility to secondary infections.

73 ent serotypes and of subsequent heterologous secondary infections.

74 ell functions that renders the host prone to secondary infections.

75 mmunity, confers nonspecific protection from secondary infections.

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

77 of infected individuals resulting in 80% of secondary infections.

78 s associated with longer hospitalization and secondary infections.

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

80 nosuppression that favors the development of secondary infections.

81 s of the mosquito's capacity to give rise to secondary infections.

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

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

84 to quantify heterogeneity in the numbers of secondary infections.

85 y infection and protects distal tissues from secondary infections.

86 in the kinetic profiles between primary and secondary infections.

87 thogen-specific, increased susceptibility to secondary infections.

88 likely responsible for initiating bloodborne secondary infections.

89 nucleoli were found to retain infectivity in secondary infections.

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

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

92 ributes to accelerated immune control during secondary infections.

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

94 y pathogens and promote host defense against secondary infections.

95 d to overcome anti-CMV immunity to establish secondary infections.

96 rion assembly and that this process prevents secondary infections.

97 laboratory-confirmed influenza, to identify secondary infections.

98 tent immunosuppression and susceptibility to secondary infections.

99 associated with increased susceptibility to secondary infections.

100 RATIONALE: Sepsis can be complicated by secondary infections.

101 protective immunity and disease severity in secondary infections.

102 with a greater propensity for opportunistic secondary infections.

103 9.1%) in the standard care group experienced secondary infections, 47 (31.1%) vs 42 (28.3%) needed in

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

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

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

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

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

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

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

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

112 y-two (55%) of 58 households had evidence of secondary infection among household contacts.

113 We found substantial evidence of secondary infections among household contacts.

114 al keratitis through their susceptibility to secondary infection and contribution to corneal resistan

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

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

117 Secondary infection and higher viremia were independent

118 In the urban site, the high rate of secondary infection and infection with the same subspeci

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

120 Our analysis suggests strong barriers to secondary infection and outbreeding amongst malaria para

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

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

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

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

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

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

127 nt of patients and guide treatments to avoid secondary infections and lower mortality.

128 ss biting habits that can lead to allergies, secondary infections and mental health issues.

129 dious onset, hypoxaemic respiratory failure, secondary infections and pulmonary fibrosis.

130 ng seems to be useful to tailor treatment of secondary infections and re-evaluate antibiotic prophyla

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

132 within the microbiota, reducing the rate of secondary infections and subsequent antibiotic use.

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

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

135 se early dengue exposure, increasing risk of secondary infection, and imply serosurveys at fine spati

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

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

138 Following secondary infection, antigen-specific BRM cells differen

139 produced a higher risk of dengue fever upon secondary infection are: DEN1 followed by DEN2; DEN1 fol

140 HIV wasting and secondary infections are also associated with increased

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

160 ons, also called polymicrobial infections or secondary infections, can further exacerbate disease.

161 g reproduction number (the average number of secondary infections caused by an infected person).

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

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

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

165 odds ratios (OR) to assess risk factors for secondary infection, defined by a positive rRT-PCR or EL

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

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

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

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

170 8 T cell populations that were induced after secondary infection displayed polyfunctionality and were

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

172 ce of cross-protection and increased risk in secondary infections due to antibody-mediated immune enh

173 and 21; and the proportion of patients with secondary infections during their ICU stay.

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

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

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

177 ic-resistance genes of E. coli isolated from secondary infections following FMD-outbreak in cattle.

178 R(0) represents the average number of secondary infections generated by one infected individua

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

180 improves, post-sepsis immunosuppression and secondary infection have increased in importance.

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

182 Enhanced secondary infections have been implicated in the majorit

183 .21, 0.42; P < 0.001) and by 59% following a secondary infection (hazard ratio = 0.41, 95% confidence

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

185 renders the infected cells nonpermissive for secondary infections.IMPORTANCE Superinfection exclusion

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

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

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

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

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

191 bacterial clearance during both primary and secondary infections in mice of the H-2(b) haplotype.

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

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

194 c prophylaxis; 33 patients (42.9%) developed secondary infections, including 14 cases (17.9%) of infe

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

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

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

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

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

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

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

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

203 ed by beta-glucan confers protection against secondary infections, its impact on autoinflammatory dis

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

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

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

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

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

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

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

211 neas with Pseudomonas aeruginosa resulted in secondary infection of ocular glands.

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

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

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

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

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

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

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

219 rates have declined precipitously from ~3.5 secondary infections per infected individual to ~1 at pr

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

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

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

223 Secondary infection predisposes individuals to more seve

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

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

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

227 hin US households and estimate the household secondary infection rate (SIR) to inform strategies to r

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

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

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

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

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

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

234 We estimated the household secondary infection risk (SIR) and serial interval (SI)

235 ed cases ranged from 3.2 to 3.6 days and the secondary infection risk ranged from 7.2% to 12.6% by ty

236 They appear, based on serial interval and secondary infection risk, to have similar transmission p

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

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

239 These secondary infections sometimes develop into systemic inf

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

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

242 s carrying genes encoding resistance against secondary infections, such as those used in phage therap

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

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

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

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

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

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

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

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

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

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

253 ng data in Hunan, China, we find that 80% of secondary infections traced back to 15% of severe acute

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

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

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

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

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

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

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

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

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

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

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

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

266 As a consequence the clinical signs of secondary infections were significantly reduced resultin

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

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

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

270 It is becoming increasingly apparent that secondary infection with a closely related flavivirus st

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

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

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

274 During secondary infection with a heterologous dengue virus (DE

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

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

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

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

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

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

281 er B cells and PCs subsequent to primary and secondary infection with helminths.

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

283 eks after diet switch, all mice were given a secondary infection with influenza PR8, and memory T-cel

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

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

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

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

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

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

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

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

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

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

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

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

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

297 ructured population and they can interact as secondary infections with primary infections.

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

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

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