ライフサイエンスコーパス: acute infection

1 evidence of CD8(+)T cell dysfunction during acute infection.

2 but not in organs typically affected during acute infection.

3 ducing potent inflammasome activation during acute infection.

4 eys that began antiretroviral therapy during acute infection.

5 HIKV may cause long-lasting arthralgia after acute infection.

6 vely prevents immunity-induced damage during acute infection.

7 ic infection and is found in some that cause acute infection.

8 subjective, as well as insensitive for early acute infection.

9 esponses to extracellular stimuli such as an acute infection.

10 fic CD8(+) T cells were equal in chronic and acute infection.

11 and enhances CDK-5 activity during lytic or acute infection.

12 functional effector T cells arising early in acute infection.

13 ategy for transmitted/founder viruses during acute infection.

14 d interferon gamma (IFN-gamma) levels during acute infection.

15 on its role as an antiviral molecule during acute infection.

16 induce innate immune responses that restrict acute infection.

17 CD4(+) T cell memory subsets at the peak of acute infection.

18 as virus-specific antibody production after acute infection.

19 esult is often interpreted as a marker of an acute infection.

20 urbations that are typically associated with acute infection.

21 in mediating emergency granulopoiesis during acute infection.

22 ef, rendering these responses ineffective in acute infection.

23 r being the major initial IL-17 producers in acute infection.

24 transiently depleted of CD8(+) cells during acute infection.

25 ulatory effect on CD8 T cell responses to an acute infection.

26 "oral flora" species represented a state of acute infection.

27 ing 5 different viruses, causing chronic and acute infection.

28 blood completely masked in membranes during acute infection.

29 imited the bacterial burden in tissues after acute infection.

30 f HRP2 antigenemia following treatment of an acute infection.

31 ersus secondary memory CD8(+) T cells during acute infection.

32 a set point in a cohort of six subjects with acute infection.

33 ersus secondary memory CD8(+) T cells during acute infection.

34 cing the progression of M. pneumoniae during acute infection.

35 ) dependent upon expression of VEGFR2 during acute infection.

36 osal immune system is overcome by SIV during acute infection.

37 at may be essential for host survival during acute infection.

38 n studies of cells in the brain that survive acute infection.

39 ze the role of the NLRP3 inflammasome during acute infection.

40 veloped as a new antitubercular aimed at the acute infection.

41 S-STING cytosolic DNA-sensing pathway during acute infection.

42 for the immune response during M. pneumoniae acute infection.

43 ivation of the innate immune response during acute infection.

44 ive replication might be a better marker for acute infection.

45 may also play a useful role in detection of acute infection.

46 T cells residing in different tissues during acute infection.

47 on and can persist for months to years after acute infection.

48 ed with Teff, supporting previous reports in acute infection.

49 ce, suggesting that rfaH is not required for acute infection.

50 rgetics of effector T cells generated during acute infection.

51 serves a beneficial function in response to acute infection.

52 ons of T/F viruses in each individual during acute infection.

53 some laboratories as an additional marker of acute infection.

54 a key reservoir established by HIV-1 during acute infection.

55 therapy (ART), but only if initiated during acute infection.

56 associated with influx into the liver during acute infection.

57 in M. tuberculosis-infected macaques during acute infection.

58 e episodes is an independent risk factor for acute infection.

59 from insufficient insulin administration and acute infection.

60 s a useful tool to discriminate chronic from acute infection.

61 e 13 into recipient mice that had cleared an acute infection.

62 alizing activity that prevents viremia after acute infection.

63 and why ART appears to be more effective in acute infection.

64 oir and the immune damage that occurs during acute infection.

65 man monoclonal antibodies (HMAbs) to prevent acute infection.

66 loads and cytokine profile during patients' acute infections.

67 t not absolute reduction in CD8 responses to acute infections.

68 of the host to respond to newly encountered acute infections.

69 its deficiency has been linked with several acute infections.

70 predictive value of 0% for the detection of acute infections.

71 uring the primary immune response to several acute infections.

72 cid amplification testing (NAAT) to identify acute infections.

73 ointestinal disorders and fatigue may follow acute infections.

74 dependent patterns of viral load dynamics in acute infections.

75 o scavenge and solubilize ferric iron during acute infections.

76 limiting damage by the immune system during acute infections.

77 pon early FAS inhibition in chronic, but not acute, infection.

78 e then ovalbumin (OVA)-sensitized during the acute infection (3-days post inoculation) and then chron

79 tions for their age in 1 of 32 subjects with acute infection (3.1%) and 10 of 32 with chronic infecti

80 We found that during acute infection, a significant host response was mounted

81 ne combo identified 12 individuals as having acute infections (Ag(+)/Ab negative [Ab(-)]); however, n

82 noncontrollers (NC), and 44 individuals with acute infection (AI) were compared.

83 rituximab-treated and untreated macaques in acute infection, analyzing individual granulomas reveale

84 ing of tissue persists despite resolution of acute infection and a 10- to 100-fold reduction in the n

85 l engulfment of presynaptic terminals during acute infection and after recovery.

86 ited immunity can provide protection against acute infection and also prevent chronic infection.

87 on (IFN-gamma) and RANTES, were increased in acute infection and also were associated with viral load

88 sponses in the inflammatory contexts of both acute infection and chronic autoimmunity in mice.

89 pidly established during the first months of acute infection and continues to increase slowly during

90 pecimens and peripheral blood B cells during acute infection and convalescence.

91 that serum acetate increases in response to acute infection and describe a mechanism by which this r

92 from seven infected adults identified during acute infection and determined the ability of the virus

93 27(+) CD19(+) cells) reached up to 8% during acute infection and early convalescence.

94 ntial therapeutic strategies for controlling acute infection and EBV-associated B-cell lymphomas.

95 In addition to detection of acute infection and immediate treatment, we established

96 ocyte activation can cause pathology both in acute infection and in exacerbations of chronic respirat

97 Viral genetic diversity was low during acute infection and increased upon progression to chroni

98 h neutrophils are the most abundant cells in acute infection and inflammation, relatively little atte

99 cells), increased with age and after severe acute infection and inversely correlated with the residu

100 Post-SIV infection, MDSC were elevated in acute infection and persisted during 7 mo of combination

101 3 cells was irreversible, which began during acute infection and persisted until terminal disease.

102 ponent of biofilms and in the choice between acute infection and persistence in the host.

103 t and survival of memory CD4(+) T cells post-acute infection and play an essential role in immune pro

104 d where the viral reservoir is seeded during acute infection and the extent to which it is susceptibl

105 g the most appropriate animal model to study acute infection and the virus-specific CD8(+) T cell (CT

106 rgeted by CD8(+) T lymphocytes (CTLs) during acute infection and therefore is included in many candid

107 ulated, immunocompetent hosts at the peak of acute infection and thus they significantly advance our

108 ebound correlated with total viraemia during acute infection and with proviral DNA at the time of ART

109 Here we focus on the competition between two acute infections and we address the role of host mobilit

110 nificant IFN-gamma ELISPOT responses in both acute-infection and relapsing patients; none of the pept

111 %) had a chronic infection, 100 (22%) had an acute infection, and 7 (2%) were not infected, and for 9

112 nal routes, replicated to high levels during acute infection, and established chronic setpoint viremi

113 le to produce IL-1beta in the airways during acute infection, and lack of this inflammatory response

114 can undergo rapid sequence evolution during acute infection, and the variant pool is typically seen

115 armaceutical treatments is limited mainly to acute infection, and there are no effective treatments f

116 rapidly replicating, similar to parasites in acute infections, and another showing little evidence of

117 truation, NSAIDs, alcohol, body temperature, acute infections, and antacids.

118 IgG2a (IgG1 in humans) can prevent acute infections, and T-bet promotes IgG2a isotype switc

119 of the world, with an estimated 390 million acute infections annually.

120 iver, and adrenal glands, common targets for acute infection, appeared histologically normal with no

121 ches in the BM whereas HSCs harvested during acute infection are motile and therefore interact with l

122 However, their kinetics and functions during acute infection are poorly understood.

123 ever, the virus-host interactions regulating acute infection are unknown.

124 Acute infections are associated with a set of stereotypi

125 Acute infections are characterized by pronounced toxin p

126 HSV-1 lytic genes, usually identified during acute infection, are uniquely expressed in the EP 60 d p

127 e-matched, whole blood studies of sepsis and acute infections as compared to healthy and/or noninfect

128 virome to better understand the dynamics in acute infection, as well as the factors that may lead to

129 erial pathogen Pseudomonas aeruginosa causes acute infections associated with significant morbidity a

130 In parallel, the mice had less acute infection-associated colitis and resolved it more

131 Of these cases, 3 had unrecognized acute infection at PrEP randomization, and 2 were HIV ne

132 Among those with acute infection at randomization to FTC/TDF, M184V or I

133 Following acute infection, BoHV-1 establishes lifelong latency in

134 The Fep system has a known role in acute infection, but it is unclear whether ferric iron u

135 ole in the NK cell antiviral response during acute infection, but it strongly impaired the generation

136 ion increased sharply and transiently during acute infection, but was reduced in blood and spleen dur

137 s were numerous within the white pulp during acute infection, but were rarely observed thereafter.

138 MP10 serves a beneficial role in response to acute infection by moderating the proinflammatory respon

139 nces were identical to those obtained during acute infection by single-genome sequencing.

140 Here we show that acute infection by the New World Junin virus (JUNV) fail

141 e in eliciting lifelong immunity to virulent acute infection by Toxoplasma gondii.

142 Acute infection by Toxoplasma is hallmarked by rapid pro

143 (+) T cell-dependent immunity that prevented acute infection by type I and type II strains of T. gond

144 Thus, acute infection can drive long term immune and microbiot

145 Here, we report that a single acute infection can have dramatic and long-term conseque

146 Interestingly, acute infections can also result in platelet breakdown a

147 e virus-induced interferon production during acute infections can contribute to airway inflammation a

148 While acute infections cause short-term tissue damage, their l

149 rospect of using nucleoside analogs to treat acute infections caused by RNA viruses represents an imp

150 CTL arise in acute infection, causing escape mutations to spread rapi

151 xpressed high levels of CD27 and CD38 during acute infection, characteristic of plasmablasts, and tra

152 netic diversity is higher in chronic than in acute infection, chronically infected immunocompromised

153 nts in the Zambia-Emory HIV Research Project acute infection cohort.

154 ing the absence of infection or a very weak, acute infection compared to that of the mouse.

155 We report the first travel-acquired Zika acute infection complicated with myocarditis imported in

156 e and lack of a specific laboratory test for acute infection complicates diagnosis and surveillance.

157 T/F variants found in acute infection contained longer U cores within the moti

158 stigated whether CTL targeting of Nef during acute infection contributes to immune control by disrupt

159 In this model, acute infection correlated with high mortality, weight l

160 on protein claudin-3 was not observed during acute infection despite significantly fewer T cells.

161 red mice (recovery defined as survival after acute infection) display impaired spatial learning and p

162 Of 14 HBV acute infection donor panels (HBV-DNA-positive/anti-HBc-

163 False-positive detection, acute infection during the window phase, and resolved or

164 -6B and -7 (HHV-6A, HHV-6B and HHV-7) cause acute infection, establish latency, and in the case of H

165 induce IFN-gamma release from CD4 T cells in acute infection, even after stimulation with virus-encod

166 r successful pathogen clearance following an acute infection, exhausted T cells secrete lower levels

167 ion, in that the virus exhibited only a mild acute infection following inoculation with no detectable

168 fluid is largely effective in discriminating acute infection from its absence and identified some spe

169 gy could be used for differentiation between acute infection from past infection and immunity.

170 Before treatment, subjects with acute infection had lower CSF NFL levels, with elevation

171 s of hepatitis C virus (HCV) clearance after acute infection, higher HCV viremia, and accelerated pro

172 th postexposure prophylaxis and treatment of acute infections, IFN-alpha14, but not IFN-alpha2, signi

173 so provide target cells for the virus during acute infection, impair CD4 T-cell recovery, and are ass

174 antibodies (Ab) for early identification of acute infections, important for targeting prevention and

175 in the bone marrow (BM) were elevated during acute infection in a phagocytic NADPH oxidase-dependent

176 (m)(2)) and hospitalization or treatment for acute infection in a prospective cohort study.

177 assess anti-genotype 1 nAb responses during acute infection in at-risk persons followed prospectivel

178 ural and nonstructural viral proteins during acute infection in bronchoalveolar lavage (BAL) fluid an

179 Transcriptomic analysis during acute infection in diabetics indicated the importance of

180 and the replication capacity of viruses from acute infection in disease progression in women who sero

181 assays and the absence of clinical signs of acute infection in donors contribute to the sporadic occ

182 Influenza A virus (IAV) causes an acute infection in humans that is normally eliminated by

183 k hepatitis virus (WHV) to induce productive acute infection in naive adult woodchucks.

184 ng and its relationship to the resolution of acute infection in respiratory tissues.

185 weight loss and sickness scores) during the acute infection in the 18-month old mice that were OVA-s

186 n relevant to Salmonella pathogenesis during acute infection in the intestine and during chronic infe

187 relationship between VZV and its host during acute infection in the sensory ganglia is not well under

188 shrew has an undetectable, or a much weaker, acute infection in the TGs.

189 Acute infection in these animals caused temporary behavi

190 However, IFN is detectable in serum during acute infection in vivo for approximately 5-7 d, which c

191 track virus-target cell interactions during acute infection in vivo, we developed rK2-PVM, bacterial

192 e in the control of virus replication during acute infection in vivo.

193 Dengue is thus an example of an acute infection in which selection pressures within infe

194 The classifier identified acute infections in 27/29 (93.1%) samples and in 6/12 (5

195 adenoviruses primarily produce self-limited acute infections in humans, these agents are associated

196 sent the standardized management of the main acute infections in patients admitted in the emergency d

197 hibit reduced virulence in a murine model of acute infection, in vitro results indicate that the O-Ag

198 cause devastating damage during chronic and acute infections; indeed, bacteria are often viewed as a

199 Acute infection is characterized by immune infiltration

200 ce to HSV-1 in the trigeminal ganglia during acute infection is conferred in part by STING and IFN-al

201 Immune evasion by HIV-1 during acute infection is critical for the establishment of lat

202 Although acute infection is mostly asymptomatic in healthy person

203 (Ags) are still presented by DCs long after acute infection is resolved.

204 The hypoferremia of acute infection is therefore a pathogen-specific, not un

205 apeutic potential of these antibodies during acute infection is unknown.

206 adaptive immune cells influence outcomes of acute infections is incompletely understood.

207 eak of IL-21 expression, observed during the acute infection, is associated with an elevated IL-21(+)

208 2 differentiation) that further explains how acute infection leads to chronic inflammatory disease.

209 ibit transition of P. aeruginosa from a more acute infection lifestyle to the biofilm phenotype.

210 have a role in spontaneous clearance during acute infection, little is known about their role in chr

211 ings by Morais da Fonseca et al. reveal that acute infections may result in permanent disruption of t

212 tive activity against planktonic bacteria in acute infection models.

213 high microsomal stabilities, although in the acute infection mouse model, just one stilbene (6-fold)

214 production in the trigeminal ganglia during acute infection, mouse mortality, or the rate of reactiv

215 ear cells from Peruvian subjects cured after acute infection (n = 9) and from patients who relapsed (

216 In response to acute infection, naive CD8(+) T cells expand, differenti

217 During acute infections, naive Ag-specific CD8 T cells are acti

218 f active gammaherpesvirus replication during acute infection of a naive host is subclinical in most i

219 KV infection in pregnant women may result in acute infection of fetal tissue and brain tissue, causin

220 active promotor and this contributed to the acute infection of macrophages.

221 ing; however, recent studies have shown that acute infection of mice with live bacteria is alone suff

222 CD8(+) effector T cells (Teff cells) during acute infection of mice with lymphocytic choriomeningiti

223 ated in virus-specific CD8(+) T cells during acute infection of mice with lymphocytic choriomeningiti

224 Here we show that following control of acute infection of mice with the myotropic Colombiana st

225 irus was passaged in cell culture and during acute infection of mice.

226 We observed decreased contractility during acute infection of neonatal mice, and persistent viral i

227 ere influenza disease is characterized by an acute infection of the lower airways that may progress r

228 .IMPORTANCE Influenza A viruses (IAVs) cause acute infection of the respiratory tract that affects mi

229 of immunity associated with survival during acute infection offers insights into correlates of prote

230 ong influence of the replication capacity in acute infection on disease progression, potentially driv

231 The disease can result from acute infection or reactivation of latent infection, in

232 In patients with acute infections or chronic inflammation, oxMIF expressi

233 During acute infection our behavior tends to change.

234 equences from HCV T/F genomes recovered from acute-infection patients, we tested whether RIG-I recogn

235 During acute infections, PD-1 is transiently expressed and has

236 thogenesis of respiratory viruses during the acute infection phase and their ability to persist under

237 ion rate reveals a mutation burst during the acute infection phase that is over 10 times faster than

238 In acute infection, pre-cART NFL levels were inversely corr

239 lication capacity of viruses isolated during acute infection predicts subsequent disease progression

240 tion antiretroviral therapy initiated during acute infection prevented intestinal disease.

241 monoclonal antibody just prior to and during acute infection protects rhesus macaques from transmissi

242 th, chronic, and EC samples; it peaked after acute infection, reached a plateau in chronic infection,

243 Depletion of IFN-gamma during acute infection reduced cardiac inflammation in MAV-1-in

244 nfluenza virus-specific antibody response to acute infection remain unclear.

245 ng the evaluation of viruses obtained during acute infection, representing the transmitted virus, a m

246 the immune system following clearance of an acute infection represents an inflection point beyond wh

247 -length T/F genomes present in plasma during acute infection resulting from atraumatic rectal inocula

248 nfection can be erroneously classified as an acute infection, resulting in serious adverse consequenc

249 e secretome of P. aeruginosa derived from an acute infection revealed hypoxia-induced repression of m

250 During acute infection, robust plasmablast responses to the inf

251 n strategies, but, remarkably, 20% to 30% of acute infections spontaneously clear prior to developmen

252 For acute infections, such as cholera, phage prophylaxis cou

253 However, during this phase of acute infection, Tetherin enhanced myeloid dendritic cel

254 We found that during mice acute infection, TgIST-deficient parasites are rapidly e

255 C) class I molecules was better preserved in acute infection than in chronic infection.

256 the diet on infection by vaccinia virus, an acute infection that begins in the respiratory tract and

257 In contrast with acute infection, the IFN-lambdaR-deficient mice generate

258 Following an acute infection, the parasite can persist within its mam

259 the evidence that vIL-10 is critical during acute infection, the role of vIL-10 during persistent in

260 response helps eliminate the virus following acute infection, the virus rapidly evolves to evade the

261 e analysed to ascertain the annual number of acute infections, the HEV genotype disposition and viral

262 Respiratory complications include acute infections, the sequelae of infection (eg, bronchi

263 a rapidly replicating tachyzoite form during acute infection to a quiescent encysted bradyzoite stage

264 Unlike acute infection, tumor growth is initially unapparent; h

265 en adults, which often leads to self-limited acute infection, vertical transmission of HBV from mothe

266 resistance among those initiating PrEP with acute infection waned rapidly after drug discontinuation

267 Acute infection was accompanied by a homogeneous signatu

268 Serum WHV collected during acute infection was compared to virions harvested from W

269 Following acute infection, we find that IFN-lambdaR1-deficient mic

270 indings are likely to be applicable to other acute infections where local activation of unconventiona

271 The Armstrong strain (ARM) of LCMV causes an acute infection, whereas its derivative, clone 13 (Cl-13

272 are crucial for subsequent immune control of acute infection, which has important implications for HI

273 CD8(+) T cells show accelerated expansion in acute infection, which is associated with increased IFN-

274 utcomes, with some individuals succumbing to acute infection while others control the pathogen as an

275 e the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells

276 During acute infection with bacteria, viruses or parasites, a f

277 set is CMV specific or is also responsive to acute infection with EBV.

278 rated into cutaneous melanoma lesions during acute infection with either virus, after a cleared vacci

279 orrespondingly required for the clearance of acute infection with influenza virus.

280 ion are fully capable of inducing productive acute infection with long-lasting high viremia.

281 aturation of memory CD8(+) T cells following acute infection with lymphocytic choriomeningitis virus

282 liferation, both in vitro and in vivo during acute infection with lymphocytic choriomeningitis virus

283 y stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus

284 During the contraction phase of an acute infection with lymphocytic choriomeningitis virus,

285 R, on B cell and CD4 T cell responses during acute infection with lymphocytic choriomeningitis virus.

286 in CD8 T cells during an immune response to acute infection with lymphocytic choriomeningitis virus.

287 antigen-specific antibody production during acute infection with lymphocytic choriomeningitis virus.

288 ersion or whether they resulted from regular acute infection with subsequent antibody loss.

289 A genome, is a human pathogen that causes an acute infection with symptoms ranging from parotitis to

290 the clinical and pathological consequence of acute infection with the obligate intracellular apicompl

291 To explore these questions, we established acute infection with the rodent pneumovirus, pneumonia v

292 e whether neurons or other CNS cells survive acute infection with this virulent virus, we developed a

293 mmunodeficiency virus (SIV) transmission and acute infection with two complementary in vivo intervent

294 We show that the course of acute infection with ZIKV in these New World monkeys res

295 layers for adaptive immune responses against acute infections with retroviruses.

296 cells demonstrated enhanced cytotoxicity in acute infection, with 2-fold increases in perforin expre

297 ected in 3 out of 7 participants during late acute infection, with a mean frequency of 0.63% for posi

298 ' sera was substantially high one year after acute infection, with a slight reduction in activity ove

299 f ICU admissions, but all recovered from the acute infection without complications.

300 d E2 are generated during the late stages of acute infection, yet their contribution to spontaneous v