ライフサイエンスコーパス: acute infection

1 e critical for intracellular survival during acute infection).

2 s and remain present more than 4 years after acute infection.

3 annual vaccination; filoviruses, a virulent, acute infection.

4 subset can be localized to skin early during acute infection.

5 ing loss weeks to months after recovery from acute infection.

6 rain parenchyma long after resolution of the acute infection.

7 which required a secondary intervention for acute infection.

8 rtly after initiating CAB LA PrEP to exclude acute infection.

9 ingly different from CD8 T cell subsets from acute infection.

10 did not affect Mtb's cell replication during acute infection.

11 ion to facilitating niche acquisition during acute infection.

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

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

14 but not in organs typically affected during acute infection.

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

16 vated CD8 T cells following resolution of an acute infection.

17 f HRP2 antigenemia following treatment of an acute infection.

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

19 is relevant for antibody-based strategies in acute infection.

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

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

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

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

24 ivation of the innate immune response during acute infection.

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

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

27 T cells residing in different tissues during acute infection.

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

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

30 rgetics of effector T cells generated during acute infection.

31 serves a beneficial function in response to acute infection.

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

33 some laboratories as an additional marker of acute infection.

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

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

36 associated with influx into the liver during acute infection.

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

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

39 from insufficient insulin administration and acute infection.

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

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

42 alizing activity that prevents viremia after acute infection.

43 imates report only the short-term effects of acute infection.

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

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

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

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

48 ducing potent inflammasome activation during acute infection.

49 eys that began antiretroviral therapy during acute infection.

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

51 vely prevents immunity-induced damage during acute infection.

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

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

54 esponses to extracellular stimuli such as an acute infection.

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

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

57 functional effector T cells arising early in acute infection.

58 ategy for transmitted/founder viruses during acute infection.

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

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

61 induce innate immune responses that restrict acute infection.

62 pose their domestic pets to the virus during acute infection.

63 e (37 kBq) was observed in a rodent model of acute infection.

64 es may be limited in their ability to detect acute infection.

65 persist in these cells for months following acute infection.

66 e that is distinct from that observed during acute infection.

67 , or if PrEP is initiated during undiagnosed acute infection.

68 ction against morbidity and mortality due to acute infection.

69 decreased "emergency hematopoiesis" after an acute infection.

70 an previously observed in in vitro models of acute infection.

71 V-1 replication or inflammatory responses to acute infection.

72 nce or establishment of chronicity following acute infection.

73 sis and are early responders to pathogens in acute infections.

74 loads and cytokine profile during patients' acute infections.

75 limiting damage by the immune system during acute infections.

76 presence of parasites in all patients during acute infections.

77 utoimmune hemolytic anemia in the setting of acute infections.

78 ood has been used to detect microbial DNA in acute infections.

79 d to protect against viruses that cause only acute infections.

80 iously observed for influenza A virus during acute infections.

81 etion system (T3SS) plays a critical role in acute infections.

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

83 rus that can be detected in the blood during acute infection(2).

84 starting antiretroviral therapy (ART) during acute infection, 2% of proviruses that persist on ART ar

85 individuals before and longitudinally during acute infection(5), we were powered within each to disco

86 ia in Sabah, Malaysia, were collected during acute infection, 7 and 28 days after drug treatment.

87 did not alter P. aeruginosa virulence during acute infections, a significant difference in pathogenic

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

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

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

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

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

93 xperimental models that better manifest both acute infection and chronic, even lifelong, disease.

94 uring pre-combination antiretroviral therapy acute infection and combination antiretroviral therapy-t

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

96 27(+) CD19(+) cells) reached up to 8% during acute infection and early convalescence.

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

98 CHDI-340246, to perturb the KP during early acute infection and followed the animals for 1 y to asse

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

100 was determined for beta7-defined subsets at acute infection and in uninfected controls.

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

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

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

104 riction of viral load in women begins during acute infection and is maintained into chronic infection

105 0 levels with RvD1 therapy in both mice with acute infection and mice with chronic infection and a de

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

107 3 cells was irreversible, which began during acute infection and persisted until terminal disease.

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

109 asii forms extracellular cords, resulting in acute infection and rapid larval death.

110 controlled parasite replication in mice with acute infection and reduced the levels of interferon gam

111 ere, we use a model of endotoxinemia to link acute infection and subsequent neutrophil activation wit

112 children typically occurs a few weeks after acute infection and the putative etiology is a dysregula

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

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

115 who initiated antiretroviral therapy during acute infection and underwent analytic treatment interru

116 ppression of parasitemia in a mouse model of acute infection, and elicited 100% animal survival after

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

118 e extensive alterations in metabolism during acute infection, and identify increases in host-derived

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

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

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

122 as "G3 abcdhij") is the predominant cause of acute infections, and older men are most at risk.

123 aeruginosa pathogenicity in chronic but not acute infections, and reveal SagS to be a promising new

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

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

126 d biomarkers of infected CD4+ T cells during acute infection are poorly defined.

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

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

129 Acute infections are associated with a set of stereotypi

130 Acute infections are characterized by pronounced toxin p

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

132 nisms of immune pathology in the lung during acute infection as well at the later stages of disease r

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

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

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

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

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

138 intima of the stifle (knee) is a target for acute infection by Ebola virus/Kikwit, Ebola virus/Makon

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

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

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

142 for the first time, the associations between acute infections by GI helminths and the faecal microbia

143 ding on virus strain and host immune status, acute infections by IAV may reach sites other than the r

144 function can be recovered and resistance to acute infection can be restored by immunization with hig

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

146 (NAATs) are the primary means of identifying acute infections caused by severe acute respiratory synd

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

148 Typhoid fever is an acute infection characterized by prolonged fever followi

149 s in men and women in a Zambian heterosexual acute infection cohort.

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

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

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

153 re liver and adipose tissue pathology during acute infection, consistent with a role in acute disease

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

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

156 f disease-specific biomarker profiles during acute infections could guide the development of innovati

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

158 endering them not widely available for rapid acute infection diagnoses at the point of care to ensure

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

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

161 markers, in patients with different types of acute infections, during active disease and remission; (

162 begins, it may potentially be used to treat acute infections (e.g. Coronavirus, EBOV, ZIKV, IAV and

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

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

165 responses that are important for controlling acute infection have not been definitively characterized

166 , the initial semen virus populations during acute infection have undergone a selective bottleneck, a

167 Patients with type 2 diseases admitted with acute infections have reduced mortality, implying that t

168 Following acute infection, herpes simplex virus 1 (HSV-1) establis

169 e aged 20-50 years, had initiated ART during acute infection (ie, Fiebig stages I-III), had been taki

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

171 ontrol is distinct from that seen during the acute infection: immune cell-depleted, long-term-infecte

172 life that are distinct from those caused by acute infection.IMPORTANCE Viral infections of neurons a

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

174 the wild type (17syn+), we found that during acute infection in cell culture, 17dmiR-H1/H6 exhibited

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

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

177 ry yellow fever immunization - the model for acute infection in humans - showing their large diversit

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

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

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

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

182 d significantly less infectious virus during acute infection in the trigeminal ganglia (TG) and brain

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

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

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

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

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

188 disease and remission; (2) the prevalence of acute infections in a cohort of consecutive patients wit

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

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

191 ly clinical diagnosis and treatment, confirm acute infections in the absence of a convalescent-phase

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

193 rovided insight into immune responses during acute infection, including additional relevant data from

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

195 Acute infection is a well-established risk factor of car

196 roadly-neutralizing plasma antibodies during acute infection is associated with HCV clearance, but th

197 As lower viremia during acute infection is associated with reduced frequency of

198 Acute infection is characterized by immune infiltration

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

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

201 Although acute infection is mostly asymptomatic in healthy person

202 Viral sequence divergence during acute infection is predominantly fueled by single-base s

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

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

205 2 differentiation) that further explains how acute infection leads to chronic inflammatory disease.

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

207 BoV1 DNA loads in nasopharynx correlate with acute infection markers.

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

209 ytic choriomeningitis virus Armstrong strain acute infection model as well as the in vitro activation

210 tive activity against planktonic bacteria in acute infection models.

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

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

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

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

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

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

217 wasting and lethal disease that occur during acute infection of immunodeficient hosts.

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

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

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

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

222 Coronavirus disease 2019 (COVID-19) is an acute infection of the respiratory tract that emerged in

223 Of 948 participants, 247 (26.1%) had an acute infection, of which 224 (23.6%) were single infect

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

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

226 While the deleterious effect of acute infection on tolerance is mainly driven by proinfl

227 ear cells and their changes in patients with acute infection over time.

228 tent hosts do not typically show symptoms of acute infection, parasites are retained in latent tissue

229 ted to CRP and IL (interleukin)-1 changes in acute infection patients.

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

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

232 he epitope specificities of anti-HCV NAbs in acute infection plasma of forty-four humans with subsequ

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

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

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

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

237 lations is critical for dissemination during acute infection, recombinant ZIKVs were generated that c

238 In patients with acute infections, regardless of concomitant QT-prolongin

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

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

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

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

243 dotoxin (TTX)-sensitive sodium currents, and acute infection significantly reduced the functional exp

244 e already been shown to cause disease during acute infection, some are associated with chronic diseas

245 fected patients recruited in the CAPRISA 002 Acute Infection Study.

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

247 d cell indices significantly declined during acute infection suggesting transient anemia, and was acc

248 During acute infections, systemic inflammation rapidly induces

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

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

251 o colonize the kidneys and spleens during an acute infection than the wild-type strain.

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

253 sitive bacterium responsible for anthrax, an acute infection that most significantly affects grazing

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

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

256 During acute infections, the risk of malignant ventricular arrh

257 els of functional antibodies increased after acute infection through 7 days after treatment but rapid

258 aturation pathway of select HIV-1 bnAbs from acute infection through neutralizing antibody developmen

259 to effector and memory states in response to acute infection, Tox-deleted TST cells failed to persist

260 We studied the role of typhoid toxin in acute infection using a randomized, double-blind S. Typh

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

262 per se can significantly prolong QTc during acute infections, via cytokine-mediated changes in K(+)

263 Acute infection was accompanied by a homogeneous signatu

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

265 The importance of studying acute infection was highlighted by the observation that

266 celeration of vascular inflammation Methods: Acute infection was mimicked by injection of a single do

267 ouse model of sleeping sickness in which the acute infection was treated but brain infection remained

268 development of HIV-specific immunity during acute infection, we evaluated the generation of virus-sp

269 ia use to adapt to biofilm-associated versus acute infections were dissected by passaging transposon

270 the Torsades de Pointes cohort, concomitant acute infections were highly prevalent (30%), despite on

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

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

273 throid maturation were down-regulated during acute infections, whereas immune response genes were up-

274 buffalo during the prolonged carriage after acute infection, which may spread to cause disease in li

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

276 The consequences of acute infection with a genetically diverse HCV populatio

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

278 -specific CD4+ T cells longitudinally during acute infection with different infection outcomes.

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

280 Acute infection with human CMV (HCMV) induces the develo

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

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

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

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

285 the regulation of CD8(+) T cell fate during acute infection with lymphocytic choriomeningitis virus.

286 persistent, chronic infection; influenza, an acute infection with multiple exposures during a lifetim

287 l numbers in the spleen were observed during acute infection with myeloid-restricted ZIKV that preclu

288 the role of the pleiotropic cytokine IL-6 in acute infection with pneumonia virus of mice (PVM), a na

289 ted with CL13 or that were convalescent from acute infection with the Armstrong (Arm) strain of LCMV.

290 x but that most of those that recovered from acute infection with the LCMV Armstrong (Arm) strain sur

291 ime, CD8(+) T(M) generated in the wake of an acute infection with the natural murine pathogen lymphoc

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

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

294 Protection from yearly recurring, highly acute infections with a pathogen that rapidly and contin

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

296 NK cells decrease following chronic, but not acute, infection with SIV.

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 1 can target low-CD4-expressing cells during acute infection yet replicates efficiently in high-CD4-e

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