ライフサイエンスコーパス: initial infection

1 s were late (285 days to 3.9 years after the initial infection).

2 plaints (age, 47 +/- 9 y; 25 +/- 10 mo after initial infection).

3 Two children demonstrated evidence of an initial infection.

4 ricidal mechanisms that remain intact during initial infection.

5 down-regulate flagella production following initial infection.

6 e later phase of infection, but early in the initial infection.

7 ntigens could be detected for days after the initial infection.

8 clearance probability if the drug inhibited initial infection.

9 on of kidney tissue for up to 247 days after initial infection.

10 or vaginal flora, in the same manner as the initial infection.

11 ral immunity to prevent the establishment of initial infection.

12 ad rapidly through the environment following initial infection.

13 ment of the fungus in plant tissue following initial infection.

14 a different HPV type within 24 months of the initial infection.

15 could help HIV enter cells and establish the initial infection.

16 er, and UV damage to the skin at the site of initial infection.

17 t persist chronically in those tissues after initial infection.

18 regardless of patient's age or intensity of initial infection.

19 in chimpanzees, died of AIDS 11 years after initial infection.

20 sal tissues are major sites of HIV entry and initial infection.

21 ias that occurred at a site distant from the initial infection.

22 ost-covid unit in Italy >= 8 weeks after the initial infection.

23 device removal and reimplantation during the initial infection.

24 erience post-COVID-19 condition months after initial infection.

25 us (EBV) has a lifelong latency period after initial infection.

26 heterologous superinfection at 21 days post-initial infection.

27 o SARS-CoV-2 remains unknown 12 months after initial infection.

28 y response to SARS-CoV-2 12 months after the initial infection.

29 versa, for at least several weeks after the initial infection.

30 , defined by symptoms lasting >4 weeks after initial infection.

31 /or viral positivity after resolution of the initial infection.

32 s early as 1.5 months or >8 months after the initial infection.

33 cell responses were retained 12 months after initial infection.

34 ion from persistent RNA detection related to initial infection.

35 for viral fusion with host cell membrane to initial infection.

36 EhV-86 was seen as early as 2 days after the initial infection.

37 , and DENV-3 occurred 325-621 days after the initial infection.

38 presenting manifestation or concurrent with initial infection.

39 ing is a major pathway for adaptation during initial infection.

40 eam to tissue sites distant from the site of initial infection.

41 t appear on leaves for months to years after initial infection.

42 differentiation in LNs draining the site of initial infection.

43 ancer, often many years to decades after the initial infection.

44 d-stage infections weeks to months after the initial infection.

45 superinfected this individual 15 weeks after initial infection.

46 than naive T (TN) cells do in response to an initial infection.

47 ze and hence inhibits replication only after initial infection.

48 s is greatest in the several years following initial infection.

49 examined mice on day 35 of life, 28 d after initial infection.

50 cy and depends only on the ability to target initial infection.

51 es do not exhibit cellular preference during initial infection.

52 ls of viral protein as long as 37 days after initial infection.

53 in pre-exposed animals that have resolved an initial infection.

54 pathy/tropical spastic paraparesis after the initial infection.

55 ride, a mediator of biofilm formation during initial infection.

56 g sequential P. aeruginosa infections during initial infections.

57 use illness at a rate equal to that seen for initial infections.

58 infected persons, as well as to prevent the initial infections.

59 were frequent and often occurred years after initial infections.

60 , rate of transmission, and the magnitude of initial infections.

61 he tissue that does not receive the primary (initial) infection.

62 he risk of reinfection within 6 months of an initial infection (12.9%) was high compared with risks i

63 women less than age 20 years at the time of initial infection, 6% were reinfected by 6 months, 11% b

64 estricted to tissues adjacent to the site of initial infection; A. brassicicola infection in systemic

65 Nine months after the initial infection, all horses were challenged intranasal

66 Such a response failed to contain the initial infection and allowed the spirochetes to dissemi

67 ntains lifelong latency in neurons following initial infection and can subsequently be reactivated to

68 Both initial infection and cell-to-cell spread by herpes simp

69 programmed death-1 (PD-1), from the time of initial infection and correlated these with HCV RNA leve

70 animals could withstand higher doses of the initial infection and developed significantly larger poo

71 tor was produced between ~3 and 6 days after initial infection and did not increase the expression of

72 d interactions that determine the outcome of initial infection and highlight immune targets for thera

73 iology and structure and its relationship to initial infection and inflammation are poorly understood

74 ate groups of BALB/c mice were drug-cured of initial infection and later reinfected and treated with

75 n individuals for periods of years after the initial infection and led to gut communities marked by h

76 anti-OVA serum IgG and IgM titers after the initial infection and marked up-regulation of activation

77 A vaccine against HIV-1 virus would block initial infection and must target conserved residues.

78 ns activation shortened the interval between initial infection and onset of cell-cell fusion associat

79 he immune mechanisms that lead to control of initial infection and prevent reactivation of latent inf

80 , skin muscle may be a key cell type for the initial infection and spread of arboviral orthobunyaviru

81 icited in the mucosa, which is a key site of initial infection and subsequent HIV-1 replication in vi

82 virus requires transgene expression for both initial infection and subsequent retrograde transsynapti

83 sal immunity may be critical to control both initial infection and the massive early spread of virus.

84 ates of viral transmissibility, clearance of initial infection and waning immunity were derived in a

85 ntrating (age, 50 +/- 8 y; 27 +/- 9 mo after initial infection) and 14 who did not have these complai

86 iagnosed at the same clinical setting as the initial infection, and 50% were diagnosed at the same ty

87 stent cardiopulmonary symptoms 9-12 mo after initial infection, and a clinical assessment compatible

88 th the drug tenofovir, which interferes with initial infection, and atazanavir, which reduces the cel

89 e mortality, readmission or death due to the initial infection, and dementia death, highlighting the

90 cludes stratification by the severity of the initial infection, and subsequent likelihood of cure, re

91 ralizing antibodies are generated late after initial infection, and the neutralizing antibody respons

92 ses at the upper respiratory mucosal site of initial infection are relatively poorly defined.

93 Initial infections are cleared but chronic infection wit

94 They are unrelated to the severity of the initial infection, are often highly symptomatic and can

95 nforce cell walls to contain the pathogen to initial infection area.

96 ted IgA knockout (IgA(-/-)) mice cleared the initial infection as effectively as wild-type mice and p

97 lear targeting of the incoming virion during initial infection, as well as assembly of progeny virion

98 in vivo complement depletion facilitates the initial infection (assayed at the 2-day time point) by a

99 sus blocks (nodes) in the city, and given an initial infection at any set of nodes, e.g. any N of pos

100 latency in peripheral ganglia following the initial infection at mucosal surfaces.

101 ernation in virus transmission to humans and initial infection at the molecular level.

102 However, factors of the initial infection attributed to the stimulation of mucin

103 SARS-CoV-2 reinfection within 90 days of the initial infection based on the clinical and laboratory c

104 In this work, we develop a model of initial infection, based on the well-known standard mode

105 e and duration of viremia (compared with the initial infection), broadened cellular immune responses,

106 plication and likely develops to contain the initial infection but allows bacterial dissemination to

107 tance to a fungal pathogen not by preventing initial infection but by limiting its spread through the

108 nduction of CD8 T cells which do not prevent initial infection but eradicate infected cells before in

109 icates that vector activity is essential for initial infection but is not necessary for continued inf

110 HIV-1-P. gingivalis complexes 2 hr after the initial infection but not in cells exposed to HIV-1 alon

111 ty of Pgl+ hosts to support a phage burst on initial infection but subsequent cycles are severely att

112 Postinoculation treatment did not block the initial infection, but we identified treatment regimens

113 ing epithelial cells, may be targets for the initial infection by HIV-1.

114 rotein-mAb364 (also termed MPV364)-prevented initial infection by hMPV and halted spread of establish

115 ulation structure within patients, confirmed initial infection by one or a few viral particles.

116 antagonistic virus-virus interaction whereby initial infection by one virus prevents subsequent infec

117 and the EBV BMRF-2 protein; and (iii) after initial infection, by virus spread directly across later

118 In endemic areas, initial infection can occur in early childhood and follo

119 ies have a pivotal role in the prevention of initial infection, cellular immune responses to HPV anti

120 between approximately 1 to 5 years following initial infection compared to 18 women with similar risk

121 e of 8.7% during the 2-year period after the initial infection compared with 4.1% among uninfected co

122 atory responses for more than 180 days after initial infection compared with convalescent controls, i

123 Importantly, by demonstrating that initial infection conditions can contribute to later rea

124 uenced from blood samples collected from the initial infection, confirming in-host persistence of Ebo

125 tive against reinfection up to 524 days post-initial infection, demonstrating possible protective imm

126 ining quiescent d109 genomes weeks after the initial infection, demonstrating the functionality of th

127 Since initial infection depends on binding of the viral envelo

128 were seen in the infected brains 7 days post initial infection despite viral clearance at this time p

129 as all animals superinfected at 35 days post-initial infection developed fulminant FMD.

130 In many disease systems, the initial infection dose impacts host morbidity and mortal

131 nes infection was primarily dependent on the initial infection dose or amount of antigen displayed, a

132 protected against PCCs in persons with mild initial infections during Delta and Omicron variant pred

133 l includes stratification by the severity of initial infection, estimates of cure, recurrence, and mo

134 hat the clonotypes persisting 3-4 years post initial infection exhibit distinct functionality compare

135 The duration of initial infection, fate of primary infection, all-cause

136 The duration of the initial infection, fate of the primary infection, all-ca

137 ing systemic infections disseminate from the initial infection focus to the target organs usually thr

138 s in the upper airways, the primary site for initial infection for most respiratory viruses, primaril

139 a median (IQR) 20.0 (18.5-22.1) months after initial infection, had reduced cognitive function compar

140 Transmitted variants that established initial infection harbored key substitutions in E1E2 out

141 T cells persist in the brain even after the initial infection has been cleared.

142 fic adaptive immunity more than 1 year after initial infection has not been well characterised.

143 IBS patients is sensitized 2 years after the initial infection has resolved.

144 Several possible routes for the initial infection have been suggested [1-6], including t

145 2, which persisted for at least 1 year after initial infection, highlights the need for research on w

146 After initial infection, HIV-1 rapidly replicated and depleted

147 During initial infection, HPV16, the most prevalent cancer-caus

148 times after infection, including the time of initial infection immediately following transmission whe

149 pse parasite genotypes were different to the initial infection in 13 of 20 (65%) mothers compared wit

150 ing manifestation or was concurrent with the initial infection in 41% and 56% of patients in the non-

151 On imaging, the site of initial infection in bacterial SBO was the external audi

152 ic and antigenic variation within 28 days of initial infection in C3H/HeN mice.

153 uctural specificities that may influence the initial infection in mammalian hosts.

154 bodies remained stable 6 and 12 months after initial infection in most individuals younger than 60 ye

155 ) antibodies were detectable 12 months after initial infection in most individuals.

156 est that increasing ASL pH might prevent the initial infection in patients with CF, and that assaying

157 role in viral immunosurveillance at sites of initial infection in response to local cDC1-derived proi

158 Recent studies suggest that initial infection in the middle ear cleft may be key to

159 pathogenetic events in Lyme arthritis, from initial infection in the skin, through infection of the

160 halus was equally successful at establishing initial infections in both host populations.

161 A substantial proportion of initial infections in both men and women are asymptomati

162 infectious cycle in vivo: in the gut during initial infection, in the liver where it replicates robu

163 responsible for most HPV-related cancers, an initial infection increases the 1-year probability of re

164 le disease recurrence to demonstrate that an initial infection induced a serum IgM and mucosal IgA re

165 t concern in human patients that survive the initial infection insult.

166 After an initial infection is introduced to a prison, the model e

167 We discovered that compared to the initial infection isolate, the strain recovered during a

168 rsistent S. aureus bacteremia cases with the initial infection isolates and with three resolved S. au

169 cancers arise years if not decades after the initial infection, it has been estimated that there will

170 In some cases, initial infection leads to chronic and reactivating bruc

171 Initial infection levels affecting less than 10 % of cel

172 ion and persistence threshold depends on the initial infection levels.

173 hile such virulence factors are important in initial infection, many become dysregulated or nonfuncti

174 eoformans cells are melanized and imply that initial infection may involve exposure to melanized cell

175 elopment of stronger immune responses to the initial infection may protect from superinfection.

176 ere disease during reinfection compared with initial infection (McNemar odds ratio, 0.2; 95% CI, 0.0-

177 Following an initial infection, MDV enters a latent state and integra

178 However, initial infection mostly occurs via CCR5, despite abunda

179 ctal CT-positive NAAT after clearance of the initial infection; none reported anal sex.

180 Initial infection occurred on the filaments, which preve

181 In addition if initial infection occurs during the growth phase then an

182 gnals produced in the local leaves where the initial infection occurs.

183 lls and showed the ability to expand from an initial infection of 1% of hypoxic cells to spread throu

184 ctiforme exist which show elevated levels of initial infection of A. punctatus as a consequence of re

185 utation in sigH resulted in a sixfold-higher initial infection of A. punctatus tissue without a paral

186 During the initial infection of B lymphocytes by Epstein-Barr virus

187 near normal numbers of target cells and the initial infection of bone marrow occurs normally in vivo

188 ecular processes that might occur during the initial infection of cells with exogenous transmissible

189 ikely need to induce antibodies that prevent initial infection of host cells or that limit early even

190 ting interactions between Env and MR reduces initial infection of macrophages by cell-free virus.

191 Prevention of the initial infection of mucosal dendritic cells (DC) and in

192 y the heretofore unknown length of time from initial infection of newly developing cluster of young l

193 self-amplify and spread in the tumor from an initial infection of only a few cells.

194 After the initial infection of peripheral tissues such as mucosal

195 of thrips, but they are not required for the initial infection of plants.

196 imulation is required for HSK but that while initial infection of TG is greater in CD28(-/-) mice, th

197 M. tuberculosis from the lung following the initial infection of the host.

198 in Vero cells could dramatically reduce the initial infection of the respiratory tract in animal mod

199 maA mutant was 10-fold less effective in the initial infection of the traumatized aortic valve.

200 primarily targets ciliated cells during the initial infection of the upper respiratory tract.

201 el derived from primary human "salispheres." Initial infection of these primary salivary cells with H

202 Our data show that, during the initial infections of epithelial cells with respiratory

203 In 1999, 18 years after the initial infection, one of the members (D36) developed AI

204 in axons to either sensory ganglia following initial infection or back out to peripheral sites of inn

205 velope proteins were not detected during the initial infection or during rechallenge.

206 ccines generate antibodies that either block initial infection or help eradicate the virus before it

207 se; however, whether it acts at the level of initial infection or in promoting clinical progression i

208 hisms may have been present from the time of initial infection or may have appeared in response to im

209 atients to be readmitted or die due to their initial infection or other lower respiratory tract infec

210 er this transformation tropism occurs during initial infection or subsequently during the cellular tr

211 te is fully infected for at least one of the initial infection patterns, find the closest, for exampl

212 endent viral amplification at local sites of initial infection, perhaps through a macrophage-dependen

213 of the inflammatory responses at the site of initial infection (peritoneal cavity) revealed that CLP

214 onsists of two major pathological phases: an initial infection phase elicited by SARS-CoV-2 entry and

215 siders room properties, mask efficiency, and initial infection probability of the occupants.

216 potentially fundamental to understanding the initial infection process, intracellular survival, virul

217 the virus, not the target cell, to abort the initial infection process.

218 ediate not only virion assembly but also the initial infection processes of cell entry and nuclear en

219 Both initial infection rate constants, k, and decay constants

220 ently within nonciliated cells despite a low initial infection rate.

221 ed infection was due to recrudescence of his initial infection rather than reinfection by another str

222 The timing of initial infection, reinfection, and the variants involve

223 After this initial infection resolves, the virus remains in a laten

224 However, the initial infection resulted in lasting elevation of antib

225 ypnozoites) that can reactivate months after initial infection resulting in relapses.

226 , we demonstrate how immune signaling during initial infection results in an epigenetic memory on HSV

227 Type I interferon (IFNalpha) exposure during initial infection results in promyelocytic leukemia nucl

228 were not stably maintained regardless of the initial infection route, which led to reductions in loca

229 ll airways disease occurred independently of initial infection severity.

230 was significantly associated with time since initial infection showing that cognitive deficits improv

231 Unknown initial infection site and 72-hour surveillance cultures

232 grammed cell death in tissue surrounding the initial infection site limits pathogen spread.

233 panied by rapid cell death in and around the initial infection site, a reaction known as the hypersen

234 wing colonization of host tissues beyond the initial infection site.

235 itment of CX3CR1(hi) patrolling monocytes to initial infection sites in the mouse.

236 lipids to regulate macrophage recruitment to initial infection sites.

237 rophils do not interact with mycobacteria at initial infection sites.

238 nt (ART) suppresses HIV replication from the initial infection stages, with further decay following l

239 t transmission of SARS-CoV-2, leading to the initial infection, stays an open question.

240 e MCC can facilitate SARS-CoV-2 spread after initial infection, subsequent MCC decreases inhibit spre

241 subtype C isolates may be less fit following initial infection (T-cell and macrophage data) and may l

242 ted girls had a shorter mean time to loss of initial infection than did HIV-infected girls (403 days

243 infection may play a more important role in initial infection than previously appreciated.

244 immunization induces immunity at the site of initial infection, the respiratory tract, thereby preven

245 After initial infection, the virus establishes latent reservoi

246 After the initial infection, the virus remains inactive or latent

247 then gradually, for the first 10 years after initial infection; the risk is relatively constant from

248 However, only in Arabidopsis did this initial infection then spread into the developing siliqu

249 r infection status, and that at the stage of initial infection there was no support for the dilution

250 ty of the urothelial barriers at the time of initial infection, these QIRs were established within te

251 d downstream impacts (tissue damage from the initial infection, tissue hypoxia, host dysbiosis, and a

252 arrier to understanding the progression from initial infection to cancer has been the lack of in vitr

253 at this virus cannot spread from the site of initial infection to neighboring cells.

254 to C. jejuni, we assessed the ability of an initial infection to prevent clinical illness after a se

255 The time from initial infection to reinfection was <1 year in 11 (41%)

256 n vary widely with respect to the outcome of initial infection to self-resolving acute or chronic dis

257 l of pathways that JCV may use from sites of initial infection to the brain.

258 scribing the sequence of events leading from initial infection to the induction of defense genes.

259 virus-laden airborne particulates, with the initial infection triggered along the respiratory pathwa

260 a target-cell-limited model from the time of initial infection until shortly after the peak in viremi

261 the receptor-binding domain 12 months after initial infection, using ELISA.

262 a result, the host's ability to control the initial infection was greatly enhanced.

263 vaccines elicited similar protection in that initial infection was not prevented, but subsequent ampl

264 elative risk of superinfection compared with initial infection was therefore 0.0 (95% confidence inte

265 urrence 1, 2, 3, 4, 5, and 6 years after the initial infection was, respectively, 13.0% (9/69), 17.4%

266 No association between chronic fatigue and initial infections was seen in primary care practices.

267 coons reveals the long lasting effect of the initial infection wave in determining how viral populati

268 After excluding initial infections, we observed 534 asymptomatic and 88

269 The SI variants that were associated with initial infection were dual tropic, with efficient repli

270 omorbidities and COVID-19 severity after the initial infection were not associated with reinfection.

271 ss demographic spectra and in patients whose initial infections were both asymptomatic/mild and moder

272 9-4.3) significantly increased the odds that initial infections were HSV-1 rather than HSV-2.

273 he pathogen abundantly expresses OspC during initial infection when the antigen is required, but down

274 ic T cells was moderately reduced during the initial infection, which might be a consequence of reduc

275 notion that OspC plays a unique role during initial infection while the antigenically variant VlsE p

276 at a person with antibodies well tuned to an initial infection will not be protected against the same

277 nd pig showed comparable susceptibilities to initial infection with a highly pathogenic avian influen

278 Furthermore, initial infection with a low dosage (10(6) CFU/ml) of L.

279 e found that PAM were readily susceptible to initial infection with all five avian and mammalian infl

280 ccine candidates potentially able to prevent initial infection with either of these two hepatotropic

281 Initial infection with HIV-1 is transmitted by macrophag

282 The timeline from initial infection with HPV to the onset of invasive cerv

283 A high incidence of initial infection with human papillomavirus (HPV) was pr

284 Weeks after an often mild or asymptomatic initial infection with SARS-CoV-2 children may present w

285 pike IgG was normalized in a few weeks after initial infection with SARS-CoV-2, indicating that the i

286 Initial infection with the BI/NAP1/027 epidemic clone wa

287 ablished cohort of 40 persons >6 years after initial infection with WNV.

288 it attenuated inflammatory responses to the initial infection, with reduced posttreatment increases

289 During initial infection, within-host HA diversity increased dr

290 6 months from initial dose (ie, clearance of initial infection without subsequent microscopically con