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1 EBOV causes hemorrhagic fever, organ damage, and shock c
2 EBOV GP vaccine with Matrix-M adjuvant is well tolerated
3 EBOV is a negative-sense RNA virus that can infect human
4 EBOV RNA was detected in semen samples from 30% of the s
5 EBOV-specific CD8+ and CD4+ T-cell responses were signif
6 EBOV-targeting antibodies cross-react with other Ebolavi
7 EBOV/Mak was inactivated (> 6 log(10)) by 70% ethanol af
8 0 samples (31.4%) versus in 21 of 70 (30.0%) EBOV-positive samples by repeat qRT-PCR (overall concord
9 of enrolled HCWs were reactive to at least 1 EBOV protein: 159 (28.1%) were seroreactive for anti-gly
10 ity improvement compared to the 53 ng mL(-1) EBOV antigen detection limit of the existing rapid EBOV
15 onducted in 230 healthy adults to evaluate 4 EBOV GP antigen doses as single- or 2-dose regimens with
18 st the potential to use Ct values from acute EBOV diagnostic specimens for index patients as an early
26 5, protects nonhuman primates (NHPs) against EBOV and SUDV infection when delivered four days post in
35 ous two-dose Ad26,MVA regimens containing an EBOV insert induce strong, durable humoral and cellular
36 search resulted in the recent approval of an EBOV-targeted vaccine by European and US regulatory agen
39 equivalent degrees of inhibition of LASV and EBOV glycoprotein (GP)-bearing pseudoviruses; three (clo
40 ug cocktail that could inhibit both LASV and EBOV.IMPORTANCE Lassa and Ebola viruses continue to caus
41 partners: PS, EBOV virus-like particle, and EBOV glycoprotein/vesicular stomatitis virus pseudovirio
44 r EBOV RNA in blood by qRT-PCR, and for anti-EBOV-specific IgM and IgG antibodies by enzyme-linked im
46 ith adjuvant showed a rapid increase in anti-EBOV GP IgG titers with peak titers observed on Day 35 r
47 ith adjuvant showed a rapid increase in anti-EBOV GP immunoglobulin G titers with peak titers observe
51 3 participants had PBMCs which produced anti-EBOV-specific IgG antibodies upon stimulation with EBOV-
52 vaccination, and then treated with the anti-EBOV GP mAb MIL77 starting 3 days postexposure show no e
59 ed the potency of eight drugs known to block EBOV entry with their potency as inhibitors of LASV entr
61 us noncoding RNAs (ncRNAs) derived from both EBOV and MARV during infection of both bat and human cel
65 ring shipping and handling, mNGS followed by EBOV-specific capture probe enrichment in a U.S. genomic
66 h the patient's blood sample was negative by EBOV qRT-PCR testing, identification of viral reads by m
68 to treat acute infections (e.g. Coronavirus, EBOV, ZIKV, IAV and measles), and also topically for the
69 le inhibitors of filovirus entry destabilize EBOV GP and uncovered evidence that the most potent inhi
72 nsor's extraordinary capability of detecting EBOV antigen at ultralow concentration compared to exist
73 antenna-based biosensor successfully detects EBOV soluble glycoprotein (sGP) in human plasma down to
74 to expand protective breadth against diverse EBOV strains and evaluated the impact of vaccine dosing
75 to 9-fold higher among recipients of 2-dose EBOV GP with adjuvant, compared with placebo on Day 35,
76 to 9-fold higher among recipients of 2-dose EBOV GP with adjuvant, compared with placebo on Day 35,
85 s replication sites correlated with enhanced EBOV disease progression in specific conditions; at a hi
88 ings from the serologic testing of blood for EBOV-specific antibodies, molecular testing for EBOV in
93 rst rigorous assessment of the potential for EBOV to encode viral miRNAs and provides evidence contra
94 y proteins act as cell surface receptors for EBOV, and that the interaction between TIM and phosphati
99 V-specific antibodies, molecular testing for EBOV in blood and semen, and serologic testing of periph
103 plexity of antibody-mediated protection from EBOV disease highlights the structural constraints of Fc
104 mplex with cleaved Ebola virus glycoprotein (EBOV GP(CL)) reveals that binding of the mAb structurall
105 vel synthetic anti-Ebola virus glycoprotein (EBOV-GP) DNA vaccines as a strategy to expand protective
107 ent in a U.S. genomics laboratory identified EBOV reads in 22 of 70 samples (31.4%) versus in 21 of 7
108 LAV belonging to a distinct genus.IMPORTANCE EBOV and MARV, members of the family Filoviridae, are hi
109 orts the concept that NK cells accumulate in EBOV-infected tissues and can contribute to viral pathog
114 studies in mice found these epitopes induce EBOV-neutralizing antibodies and protect against lethal
120 A chimeric VSV expressing the full-length EBOV GP (VSV-EBOV) containing the MLD was substantially
121 d CD4+ T-cell responses in 37 Sierra Leonean EBOV disease survivors with (n = 19) or without (n = 18)
125 ) could fully protect ferrets against lethal EBOV, SUDV, and BDBV infection, and a single 25-mg/kg do
130 and Rousettus cells, MLAV VP35 behaved like EBOV and MARV VP35s, inhibiting virus-induced activation
132 ivity, specificity and correlation with live EBOV neutralisation were greater for the VSV-based pseud
135 a marked increase in antibody titers to most EBOV proteins and affinity maturation to GP is associate
136 to determine seroprevalence against multiple EBOV antigens among HCWs of Boende Health Zone, Democrat
137 the trivalent vaccine bound and neutralized EBOV and SUDV at equivalent levels and BDBV at only a sl
139 ue culture infectious dose(50) (TCID(50)) of EBOV/Mak was exposed to DAL at ambient temperature.
140 disease outbreaks, as well as the ability of EBOV to persist in the environment under certain conditi
143 s challenged with a uniformly lethal dose of EBOV one day following vaccination, and then treated wit
148 es targeted to EBOV GP; however, handling of EBOV is limited to containment level 4 laboratories.
150 The rapid and substantial inactivation of EBOV/Mak by DAL suggests that use of this hygiene produc
151 lts demonstrate >= 6 log(10) inactivation of EBOV/Mak dried on prototypic surfaces by EDS or formulat
152 genesis studies confirmed that inhibition of EBOV viral entry is mediated by the direct interaction w
155 this review, we describe the pathogenesis of EBOV and summarize the current status of EBOV vaccine de
164 and lymphatic organs are important sites of EBOV infection and that dysregulating the function of th
169 es harboring surface glycoprotein trimers of EBOV-Zaire/Makona produced anti-Ebola IgG polyclonal ant
173 m a screen of FDA-approved drugs as a potent EBOV viral entry inhibitor, via binding to EBOV glycopro
174 in all vaccinees, we detected highly potent EBOV-neutralizing antibodies with activities comparable
177 IM-4 and the following binding partners: PS, EBOV virus-like particle, and EBOV glycoprotein/vesicula
179 e safety and immunogenicity of a recombinant EBOV glycoprotein (GP) nanoparticle vaccine formulated w
180 e safety and immunogenicity of a recombinant EBOV glycoprotein (GP) nanoparticle vaccine formulated w
184 for inactivating Ebola virus-Makona strain (EBOV/Mak) on stainless-steel carriers per ASTM E2197-11.
186 hibitor development and refinement targeting EBOV.IMPORTANCE The most recent Ebola virus disease outb
193 uman monoclonal antibodies (mAb) against the EBOV GP have shown promise in animals and humans when ad
195 mimics the conserved interaction between the EBOV GP core and its glycan cap beta17-beta18 loop to in
198 icular stomatitis virus (VSV) expressing the EBOV glycoprotein (GP) might selectively target brain tu
202 RNA synthesis in an individual patient, the EBOV genome exists around a dominant viral genome sequen
203 monoclonal antibodies (mAbs) that target the EBOV glycoprotein (GP) have demonstrated potent protecti
205 tide on viral replication and found that the EBOV polymerase initiates replication opposite the 3'-CC
207 imeric vesicular stomatitis viruses with the EBOV glycoprotein substituted for the VSV glycoprotein s
208 t mice when the MLD was expressed within the EBOV glycoprotein than when EBOV lacked the mucin-like d
209 , and VP24 proteins were compared with their EBOV and MARV homologs for innate immune pathway modulat
210 anged from 40 to 100 pN, suggesting that TIM-EBOV interactions are mechanically comparable to previou
211 dings, the biophysical properties of the TIM-EBOV interaction, such as the mechanical strength of the
217 tivity to the protective function of mAbs to EBOV GP, we selected anti-GP mAbs targeting representati
219 with mutations in GNPTAB, are refractory to EBOV, whereas cells from their healthy parents support i
221 a longitudinal study of B cell responses to EBOV in four survivors of the 2014 West African outbreak
223 o assess neutralising antibodies targeted to EBOV GP; however, handling of EBOV is limited to contain
224 closer relationship of MLAV to MARV than to EBOV but also are consistent with MLAV belonging to a di
225 ncRNAs from both viruses, we identified two EBOV ncRNAs in our sequencing data that were near-matche
226 activating Ebola virus (Makona C07 variant) (EBOV/Mak) within an organic load in suspension was evalu
227 entifying drugs that block both Ebola virus (EBOV) and Lassa virus (LASV), two unrelated but highly p
228 SHERLOCK) diagnostics targeting Ebola virus (EBOV) and Lassa virus (LASV), with both fluorescent and
229 viridae Because the filoviruses Ebola virus (EBOV) and Marburg virus (MARV) modulate host innate immu
230 quencing (mNGS) to detect Zaire Ebola virus (EBOV) and other potential pathogens from whole-blood sam
232 glycoproteins (GPs) from Zaire Ebola virus (EBOV) and Sudan Ebola virus (SUDV) and is designed to ex
245 re more likely to be exposed to Ebola virus (EBOV) during an outbreak compared to people in the gener
246 rtemisinin, the beneficial anti-Ebola virus (EBOV) effect observed could possibly be attributed to th
249 e the most recent outbreak, the Ebola virus (EBOV) epidemic remains one of the world's public health
251 is virus vaccine expressing the Ebola virus (EBOV) glycoprotein (GP) (rVSV-ZEBOV) was successfully us
252 Since its discovery in 1976, Ebola virus (EBOV) has caused numerous outbreaks of fatal hemorrhagic
253 icacy against the highly lethal Ebola virus (EBOV) in humans is almost impossible due to obvious ethi
255 can mediate protection against Ebola virus (EBOV) infection through direct neutralization as well as
260 s for household transmission of Ebola virus (EBOV) is important to guide preventive measures during E
261 Evidence from the 2013-2016 Ebola virus (EBOV) outbreak indicated that different genotypes of the
262 viral pathogenicity.IMPORTANCE Ebola virus (EBOV) outbreaks can claim numerous lives and also devast
264 antibody repertoire against the Ebola virus (EBOV) proteome was characterized in an acutely infected
265 Ebola virus disease.IMPORTANCE Ebola virus (EBOV) remains a high-priority pathogen since it continue
268 versus nontargeted violence on Ebola virus (EBOV) transmission in Democratic Republic of the Congo (
270 member of the Ebolavirus genus, Ebola virus (EBOV), and ineffective against outbreak-causing Bundibug
271 fusion proteins including HIV, Ebola virus (EBOV), influenza A virus (IAV) and Epstein Barr virus (E
272 ead by close contact, including Ebola virus (EBOV), severe acute respiratory syndrome coronavirus (SA
279 ous study in which we used an attenuated VSV-EBOV with no MLD that expressed green fluorescent protei
283 VSV expressing the full-length EBOV GP (VSV-EBOV) containing the MLD was substantially more effectiv
288 tients (64.5%) tested in Kinshasa, DRC, were EBOV positive by quantitative reverse transcriptase PCR
290 Here, we compared chimeric VSVs in which EBOV GP replaces the VSV glycoprotein, thereby reducing
293 rs (HCWs) have elevated risk of contact with EBOV-infected patients, particularly if safety precautio
294 protected against subsequent infection with EBOV and that neutralising antibodies to the viral surfa
295 virus was detected in cells inoculated with EBOV/Mak exposed to NaOCl (0.5% or 1%), PCMX (0.12% to 0
298 howed strong cross-neutralization of 2 Zaire EBOV strains (Gabon 2001 and Makona) and in vivo 3 or 5
299 and binding antibodies using wild-type Zaire EBOV (ZEBOV) or pseudovirion assays were 3- to 9-fold hi