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1 EBOV GP and RABV GP-specific antibody titers increased e
2 EBOV RNA and infectious EBOV was detected by real-time R
3 EBOV RNA was not detected in general ward spaces.
4 We present sequence data and analysis of 142 EBOV samples collected during the period March to Octobe
12 in a single injection at 1 or 24 hours after EBOV exposure or with 2 injections, half the dose at eac
13 animals may boost protective responses after EBOV challenge by maintaining transcriptional changes.
18 argeted for therapeutic intervention against EBOV infection.IMPORTANCE EBOV belongs to a family of hi
19 ate that EBOTAb conferred protection against EBOV when given post-exposure and should be explored and
20 al for rVSV-EBOV mediated protection against EBOV; however, the mechanisms by which this vaccine indu
21 hat EBOTAb is an effective treatment against EBOV disease, even when delivered late after infection.
26 able, we assessed protection conferred by an EBOV vaccine composed of vesicular stomatitis virus pseu
27 ed by post, and samples were tested using an EBOV IgG capture assay that detects IgG to Ebola glycopr
28 his small animal model for studying BDBV and EBOV using wild-type isolates and will accelerate effort
35 ed nucleobase were critical for optimal anti-EBOV potency and selectivity against host polymerases.
37 ion effort identified 4b (GS-5734) with anti-EBOV EC50 = 86 nM in macrophages as the clinical candida
42 cular stomatitis virus pseudovirions bearing EBOV glycoprotein (EBOV GP/VSVDeltaG), we evaluated viru
43 BD, we also tested whether VSVDeltaG bearing EBOV GPs that lack GP1 N-linked glycans provided effecti
44 physical and functional interaction between EBOV VP40 (eVP40) and WWP1, a host E3 ubiquitin ligase t
48 capable of partially neutralizing a chimeric EBOV carrying BDBV GP in which expression of sGP was dis
51 cells (macrophages/monocytes) as the cryptic EBOV reservoir cells in the vitreous humour and its imme
65 ultiple viruses, including Zaire ebolavirus (EBOV), Rift Valley fever virus (RVFV), Venezuelan equine
66 e that adopting miniaturized electrochemical EBOV immunosensing can detect virus level at pM concentr
67 s that regulate replication of eGFP-encoding EBOV minigenomic RNA and identified heat shock cognate p
68 riguingly, we also found that TRIM6 enhances EBOV polymerase activity in a minigenome assay and TRIM6
76 a potential supportive treatment option for EBOV disease.IMPORTANCE Emerging infectious diseases are
78 ll lines, indicating that permissiveness for EBOV at cell and organism levels do not necessarily corr
79 ses demonstrated 100% correct reactivity for EBOV and SUDV and no cross-reactivity with relevant path
81 experienced symptoms did not get tested for EBOV at the time, suggests a need to review and standard
83 ently no approved vaccines or treatments for EBOV, a better understanding of the biology and function
86 pared the interactions of VP24 proteins from EBOV and two members of the Ebolavirus genus, Bundibugyo
87 ons (iSNVs) from deep-sequenced samples from EBOV-infected patients, through a well-tailored bioinfor
88 We have identified a novel and functional EBOV VP40 interactor, ITCH, that regulates VP40-mediated
89 rus pseudovirions bearing EBOV glycoprotein (EBOV GP/VSVDeltaG), we evaluated virus binding and entry
90 geting the Ebola virus surface glycoprotein (EBOV GP) are implicated in protection against lethal dis
92 es were associated with significantly higher EBOV replication in the liver but not in the spleen, sug
97 -specific residues were also found to impact EBOV entry, with a total of 8 mTIM-4 and 14 hTIM-4 IgV d
98 available for clinical evaluation.IMPORTANCE EBOV hemorrhagic fever is one of the most lethal viral i
99 tervention against EBOV infection.IMPORTANCE EBOV belongs to a family of highly pathogenic viruses th
100 t ER-phagy is an important limiting event in EBOV replication in mouse cells and may have implication
102 The viremia level was elevated 10-fold in EBOV-C05-infected animals, compared with EBOV-C07- or EB
109 ve TLR4-mediated proinflammatory response in EBOV infection should be considered as a potential suppo
110 protein 30 (eVP30) plays a critical role in EBOV transcription initiation at the nucleoprotein (eNP)
114 vious results, MDMs treated with inactivated EBOV and Ebola virus-like particles (VLPs) induced NF-ka
121 cells have reduced replication of infectious EBOV, suggesting that VP35 hijacks TRIM6 to promote EBOV
123 f FILORAB1 to 100% protection against lethal EBOV challenge, with no to mild clinical signs of diseas
125 Remarkably, 77% of the mAbs neutralize live EBOV, and several mAbs exhibit unprecedented potency.
126 has an improved signal-to-noise ratio at low EBOV RNA concentrations and is somewhat more sensitive t
127 ked glycans on GP1 protected mice against ma-EBOV challenge, but these mutants were no more effective
129 effective immunity against challenge with ma-EBOV or a more distantly related virus, Sudan virus.
134 d Scientific Research established a national EBOV diagnostic site at the University of Sciences, Tech
135 e mined the human immune response to natural EBOV infection and identified mAbs with exceptionally po
136 on of EBOV replication and protected 100% of EBOV-infected animals against lethal disease, ameliorati
137 infectivity may have enhanced the ability of EBOV to transmit among humans and contributed to the wid
140 rapid, user-friendly assay for detection of EBOV RNA in semen that is deployable to multiple sites a
142 more natural routes require higher doses of EBOV to produce disease or that there may be differences
143 V1) expressing the membrane-anchored form of EBOV glycoprotein GP, as an intranasal (i.n.) EBOV vacci
144 nderstanding of the biology and functions of EBOV-host interactions that promote or inhibit viral bud
145 plex with the cleaved glycoprotein (GPcl) of EBOV, both determined by single-particle electron cryomi
148 t was initiated correspond to when levels of EBOV are detectable in the circulation and thus mimic wh
149 tested in the stringent guinea pig model of EBOV disease, EBOTAb has been shown to confer protection
150 promising results in the guinea pig model of EBOV infection, EBOTAb was tested in the cynomolgus maca
154 on conferred correlated with the quantity of EBOV GP-specific Ig produced but not with the production
155 3 ligases, ubiquitination, and regulation of EBOV VP40-mediated egress.IMPORTANCE Ebola virus (EBOV)
156 th mucosal surfaces is an important route of EBOV spread during a natural outbreak, and aerosols also
157 An important mechanism for the severity of EBOV infection is its suppression of innate immune respo
158 t, to our knowledge, unliganded structure of EBOV GP, and high-resolution complexes of GP with the an
160 12 days resulted in profound suppression of EBOV replication and protected 100% of EBOV-infected ani
161 ousette bat (Rousettus aegyptiacus); that of EBOV is unknown but believed to be another bat species.
163 following the cross-species transmission of EBOV from an animal reservoir, most likely bats, into hu
169 ost innate immune response to either MARV or EBOV infection in bat and human cells and the role of vi
172 onkeys could serve as a model for persistent EBOV infection in humans, and we demonstrate that promis
173 conclusion, our data suggest that persistent EBOV infection in rhesus monkeys could serve as a model
174 aboratory investigations revealed persisting EBOV RNA in the mother's breast milk and the father's se
182 important host cellular factor that promotes EBOV replication, and future studies will focus on wheth
186 ished that antibodies are essential for rVSV-EBOV mediated protection against EBOV; however, the mech
193 mouse and non-human primates which survived EBOV challenge, ELISA, western blot, mass spectrometry a
200 hematopoietic-driven immunity, to show that EBOV primarily infects CD11b(+) DCs in non-lymphoid and
210 in amino acid sequence, such as A82V in the EBOV glycoprotein (GP) that occurred early in the 2013-1
211 hat specific amino acid substitutions in the EBOV GP have increased tropism for human cells, while re
212 h the previously determined structure of the EBOV FL through several critical aromatic residues.
213 e thought to shield conserved regions of the EBOV GP receptor-binding domain (RBD), thereby blocking
215 n analysis of the secondary structure of the EBOV minigenomic RNA indicates formation of a small stem
216 n return, had OFSs that were reactive on the EBOV IgG capture assay, with similar results on plasma.
220 s for the management of possible exposure to EBOV, and for the management of illness, across organisa
222 his study, we dissected the host response to EBOV and RESTV infection in primary human monocyte-deriv
225 ndividuals who are especially susceptible to EBOV replication is possibly one of the many challenges
229 nd lack of licensed antivirals and vaccines, EBOV is listed as a tier 1 select-agent risk group 4 pat
230 n a genus distinct from that of Ebola virus (EBOV) (genera Marburgvirus and Ebolavirus, respectively)
231 have shown that the filoviruses Ebola virus (EBOV) and Marburg virus (MARV) suppress DC maturation in
234 mmune responses in survivors of Ebola virus (EBOV) and Sudan virus (SUDV) infections have provided th
238 nment limited the 2014 Nigerian Ebola virus (EBOV) disease outbreak to 20 reported cases and 8 fatali
239 The 2013-2016 West African Ebola virus (EBOV) disease outbreak was the largest filovirus outbrea
241 Aware of the rapid spread of Ebola virus (EBOV) during the current West African epidemic, Mali too
245 ted one nonsynonymous mutation, Ebola virus (EBOV) glycoprotein (GP) mutant A82V, for its effect on v
247 and efficacious vaccine against Ebola virus (EBOV) has proven elusive so far, but various inventive s
250 onhuman primate (NHP) models of Ebola virus (EBOV) infection primarily use parenteral or aerosol rout
251 al in which the patient cleared Ebola virus (EBOV) infection without experimental drugs allowed for t
252 disappointing in tests against Ebola virus (EBOV) infection, more recently, specific molecules have
253 ils ZMapp(TM) and MIL77 against Ebola virus (EBOV) infections have reignited interest in antibody-bas
254 promise for treatment of lethal Ebola virus (EBOV) infections, but their species-specific recognition
255 VP40-mediated egress.IMPORTANCE Ebola virus (EBOV) is a high-priority, emerging human pathogen that c
261 whether treatment selected for Ebola virus (EBOV) mutations conferring resistance, viral sequencing
265 Despite sporadic outbreaks of Ebola virus (EBOV) over the last 4 decades and the recent public heal
268 ent studies have suggested that Ebola virus (EBOV) ribonucleic acid (RNA) potentially present in the
272 Ferrets were also infected with Ebola virus (EBOV) to confirm their susceptibility to another filovir
274 or transmission of West African Ebola virus (EBOV) variants, which are divergent from their Central A
276 (RABV) vectored vaccine against Ebola virus (EBOV), a major threat to wild chimpanzees and gorillas.
278 ridae family that also includes Ebola virus (EBOV), causes lethal hemorrhagic fever with case fatalit
279 fection of mammalian cells with Ebola virus (EBOV), Tacaribe arenavirus, and human herpesvirus 8 (HHV
280 s against the highly pathogenic Ebola virus (EBOV), the cellular mechanisms involved in EBOV infectio
283 cosylated glycoprotein spike of Ebola virus (EBOV-GP1,2) is the primary target of the humoral host re
284 treated groups of animals with 1 dose of VSV-EBOV either in a single injection at 1 or 24 hours after
285 high-volume air sampler to determine whether EBOV could be detected during 3 independent studies with
289 in MARV survivors share characteristics with EBOV and SUDV infections but have some distinct differen
294 mbinant VSV where G protein is replaced with EBOV GP (rVSV-EBOV) is safe and highly efficacious.
296 selected SG proteins are sequestered within EBOV inclusions, where they form distinct granules that
297 iginal Xpert EBOV assay), the modified Xpert EBOV assay demonstrated greater sensitivity than the com
299 se chain reaction assays, and original Xpert EBOV assay), the modified Xpert EBOV assay demonstrated
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