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1 SARS-CoV-2 has a zoonotic origin and was transmitted to
2 SARS-CoV-2 has been detected in the CSF of some patients
3 SARS-CoV-2 infection is characterized by peak viral load
4 SARS-CoV-2 is a new member of the betacoronavirus genus
5 SARS-CoV-2 is responsible for the development of coronav
6 SARS-CoV-2 MA caused more severe disease in aged mice, a
7 SARS-CoV-2 may modulate macrophage-mediated inflammation
8 SARS-CoV-2 spike glycoprotein (S)-reactive antibodies we
9 SARS-CoV-2 viral loads, especially plasma viremia, are a
10 SARS-CoV-2 was detected by RT-qPCR and viral culture; th
11 SARS-CoV-2-specific memory CD8(+) T cells exhibited func
12 SARS-CoV-2-specific T cell responses were driven by TCR
13 SARS-CoV-2-uninfected donor sera exhibited specific neut
15 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and an existing pandemic of metabolic diseas
16 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the risk of subsequent reinfection remai
17 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are being expedited through preclinical and
18 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) based on reverse transcriptase polymerase ch
19 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in China and rapidly spread worldwid
20 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in December 2019(1,2) and is respons
21 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has elicited an equally rapid response aimin
22 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in populations, and to verify the developmen
23 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the environment are summarized and discus
24 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into Scotland using a combined phylogenetic
25 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of an ongoing pandemic that has
26 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of the currently un
27 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be required to end the coronavirus disea
28 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has devastated global public health
31 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia patients indicate that a cytokine
32 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) prevalence and the case-fatality rate during
33 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA in respiratory samples is the standard m
34 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein, used in a combined cocktail (
35 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that results in excessive inflammation and r
36 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission networks became established in
37 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causes a pathogenic condition that has been
38 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in late 2019 and has since become a
39 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a member of the Coronaviridae family of
40 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease
41 re acute respiratory syndrome coronavirus 2 (SARS-CoV-2), while striving to find a suitable vaccine t
44 re acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection increase the risk for acute nonisc
45 to both wild-type (D614) and D614G mutant(2) SARS-CoV-2 as well as CD8(+) T cell responses, and prote
47 m for detection of antibodies to SARS-CoV-2, SARS-CoV-1, MERS, three circulating coronavirus strains
48 spike D614G substitution in the USA-WA1/2020 SARS-CoV-2 strain, and found that it enhances viral repl
49 ere, with a focus on Israel, we sequence 212 SARS-CoV-2 sequences and use them to perform a comprehen
55 globally distributed haplotypes from 15,789 SARS-CoV-2 genomes and model their success based on thei
57 ut serological assays (HTSAs) and the Abbott SARS-CoV-2 IgG assay quantify levels of antibodies that
58 ify convergence of antibody sequences across SARS-CoV-2-infected patients, highlighting stereotyped n
63 ent and to treat the acute lung injury after SARS-CoV-2 infection, especially for those with the ACE
67 S adult population formed antibodies against SARS-CoV-2, and fewer than 10% of those with antibodies
69 n of commercial antibodies generated against SARS-CoV spike protein and nucleoprotein, double strande
72 titres are sufficient for protection against SARS-CoV-2 in rhesus macaques, and that cellular immune
73 D8(+) T cell responses, and protects against SARS-CoV-2 infection in the lungs and noses of mice with
77 he origin and emergence of its causal agent, SARS-CoV-2, in the human population remains mysterious,
83 ute respiratory syndrome coronavirus 2 (anti-SARS-CoV-2) antibodies provide one method for estimating
84 t individuals who were seronegative for anti-SARS-CoV-2 antibodies targeting spike (S) and nucleoprot
85 research needs pertaining to the use of anti-SARS-CoV-2 antibody tests for diagnosis, public health s
86 and subsequently tested with samples of anti-SARS-CoV-2 monoclonal antibody CR3022 (0.1 mug/ml, 1.0 m
90 odies was able to potently inhibit authentic SARS-CoV-2 infection at a concentration as low as 0.007
91 port the molecular assembly of the authentic SARS-CoV-2 virus using cryoelectron tomography (cryo-ET)
92 ing model to analyze the correlation between SARS-CoV-2 test results and 20 routine laboratory tests
93 ad nanobody candidate, NIH-CoVnb-112, blocks SARS-CoV-2 spike pseudotyped lentivirus infection of HEK
94 ctivator of transcription signaling, boosted SARS-CoV-2 replication in the IFN-competent Calu-3 cells
98 f neutralizing antibodies (nAbs) elicited by SARS-CoV-2 infection is crucial for understanding immune
99 strains of mice are not readily infected by SARS-CoV-2 because of species-specific differences in th
100 ntify host factors required for infection by SARS-CoV-2 and seasonal coronaviruses, we designed a foc
103 polymerase (RdRp) are the best characterized SARS-CoV-2 targets and show the highest degree of conser
105 onstrate that even under extreme conditions, SARS-CoV-2 virus is unable to replicate in these mosquit
110 dies have shown that, similarly to SARS-CoV, SARS-CoV-2 utilises the Spike glycoprotein on the envelo
113 inical isolate, the infectious-clone-derived SARS-CoV-2 (icSARS-CoV-2) exhibited similar plaque morph
114 portable and real-time POC device to detect SARS-CoV-2 from VTM samples using an additively manufact
116 c people were less likely to have detectable SARS-CoV-2 in NTS collected at enrollment (8/13 [62%] vs
117 lateral flow immunoassay test that detected SARS-CoV-2 immunoglobulin G (IgG) and immunoglobulin M (
118 rovide a complementary method of determining SARS-CoV-2 infection status, based on a fully independen
120 tic introduction of at least seven different SARS-CoV-2 lineages into California, including epidemic
121 While essentially all patients displayed SARS-CoV-2-specific antibodies and virus-neutralization
122 sessed risk and incidence rate of documented SARS-CoV-2 reinfection in a cohort of laboratory-confirm
123 N-gamma protected mice from mortality during SARS-CoV-2 infection, sepsis, hemophagocytic lymphohisti
125 wed robust induction of chemokines following SARS-CoV-2 infection, similar to what is seen in patient
126 acturers have developed molecular assays for SARS-CoV-2 under the Food and Drug Administration (FDA)
128 ic and symptomatic HCWs testing positive for SARS-CoV-2 rapidly declined to near-zero between 25th Ap
129 9 of the 640 throat swabs were positive for SARS-CoV-2 RNA by quantitative PCR, suggesting community
134 liva offered sensitivity and specificity for SARS-CoV-2 detection comparable to that of the current s
138 , 433 (64.8%) had previously been tested for SARS-CoV-2 RNA, and 50.0% had a positive RT-PCR result.
139 protein-reactive T cell lines generated from SARS-CoV-2-naive healthy donors responded similarly to t
140 uld potentially be developed to protect from SARS-CoV-2 and some other SARS-like viruses that might s
141 non-structural and accessory) proteins from SARS-CoV-2 using predictive algorithms to identify poten
142 emergence, plus 64 pandemic-era samples from SARS-CoV-2 PCR-negative patients with respiratory sympto
143 RS-CoV-2 Spike-pseudotyped virus and genuine SARS-CoV-2 infections are generally restricted by human
144 pants with acute smell and/or taste loss had SARS-CoV-2 antibodies; of these, 39.8% (n = 175) had nei
151 ecific CD8(+) T cells and were detectable in SARS-CoV-2 convalescent individuals who were seronegativ
152 ted benefits of lung function improvement in SARS-CoV infections, it has been hypothesized that the b
153 equencies of alternative viral infections in SARS-CoV-2 RT-PCR-negative PUIs (n = 30) and viral coinf
154 with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh the risks and at the very least
155 table using a flow cytometry-based method in SARS-CoV-2-uninfected individuals and were particularly
157 he absence of the polybasic cleavage site in SARS-CoV-2 did not affect virus replication in Vero or V
158 centers in March through May 2020, including SARS-CoV-2 testing, well-child visits, HbA(1c) testing,
160 like other closely related viruses including SARS-CoV and Middle East respiratory syndrome coronaviru
161 apacity and fate of pre-existing and induced SARS-CoV-2-specific CD8(+) T cell responses during the n
162 ex vivo analysis of pre-existing and induced SARS-CoV-2-specific CD8(+) T cells, applying peptide-loa
163 plicated in human betacoronavirus infection (SARS-CoV-2, SARS-CoV, MERS-CoV, seasonal coronaviruses).
164 ce stability was assessed using infectivity, SARS-CoV-2 survived on stainless steel, plastic, and nit
165 sults reveal possible mechanisms influencing SARS-CoV-2 infectivity and COVID-19 clinical outcomes.
166 omycin were confirmed to effectively inhibit SARS-CoV-2 replication in vitro with EC50 values of 0.00
167 potential therapies and vaccines to inhibit SARS-CoV-2 infection and ameliorate disease is the lack
168 brain organoids as a platform to investigate SARS-CoV-2 infection susceptibility of brain cells, mech
173 evidence that complement function modulates SARS-CoV-2 infection outcome, the data point to putative
178 019 (COVID-19), which is caused by the novel SARS-CoV-2, continues to spread rapidly around the world
185 cm(-2), respectively, toward detection of SARS-CoV-2 in biological media, while blind clinical eva
189 , and be a key component in the evolution of SARS-CoV-2 with this structural loop affecting virus sta
190 ntial to chart the architectural features of SARS-CoV-2 and pinpoint regions that merit focused study
192 ospitals from becoming independent 'hubs' of SARS-CoV-2 transmission, and illustrate how, with approp
193 y and on projections of the global impact of SARS-CoV-2 on the human population, and assess its plaus
195 of age and females had a lower incidence of SARS-CoV-2 infection than adolescents or adults and male
196 D-19 showed a highly significant increase of SARS-CoV-2-specific serum IgA and IgG titers after sympt
202 ), S1+S2, nucleocapsid, and ORF6 to ORF10 of SARS-CoV-2, to the HCoV-OC43 and HCoV-HKU1 betacoronavir
203 ilding on knowledge of previous outbreaks of SARS-CoV-1 and Middle East respiratory syndrome (MERS),
205 ortant for understanding the pathogenesis of SARS-CoV-2, vaccine development, and therapeutic testing
209 Antibody to the nucleocapsid protein of SARS-CoV-2 is more sensitive than spike protein antibody
210 s study characterizes the trends in rates of SARS-CoV-2 positive test results among individuals in th
212 coated with receptor binding domain (RBD) of SARS-CoV-2 spike protein, and subsequently tested with s
213 Low copy numbers (>=500 copies/reaction) of SARS-CoV-2 RNA were consistently detected by the multipl
214 p of ISMs to phylogenetic reconstructions of SARS-CoV-2 evolution, and therefore, ISMs can play an im
217 lity score that predicts an elevated risk of SARS-CoV-2 infection for multiple species including hors
218 possible postpandemic circulating season of SARS-CoV-2 and add to the knowledge pool necessary for p
219 udy aimed to determine the seroprevalence of SARS-CoV-2 antibodies in a community-based population wi
222 Despite the ability to dampen the spread of SARS-CoV-2, the causative agent of the diseases, through
231 ses (CoVs) identified in bats and pangolins, SARS-CoV-2 harbors a polybasic furin cleavage site in it
236 ing and contact tracing could have prevented SARS-CoV-2 outbreaks from becoming established in these
237 All MIS-C patients had evidence of prior SARS-CoV-2 exposure, mounting an antibody response with
238 noids from hiPSCs and showed that productive SARS-CoV-2 infection of these organoids is associated wi
241 n SARS-CoV-2, as well as the closely related SARS-CoV-1 and MERS coronaviruses, is restricted to BSL-
242 tourists and a family of 5 French residents; SARS-CoV-2 was detected in 5 individuals in France, 6 in
243 hage libraries that specifically bind the S1 SARS-CoV-2 spike protein, and block the interaction with
244 our findings provide evidence for selective SARS-CoV-2 neurotropism and support the use of hiPSC-der
248 patient samples enabled us to estimate that SARS-CoV-2 was introduced to Scotland on at least 283 oc
255 e 2019 (COVID-19), the illness caused by the SARS-CoV-2 virus, is rapidly spreading throughout the wo
256 e present a self-amplifying RNA encoding the SARS-CoV-2 spike protein encapsulated within a lipid nan
257 CoV (MERS-CoV), bat CoV HKU5 expressing the SARS-CoV-1 spike, and vesicular stomatitis virus (VSV) e
263 leavage contributes to the activation of the SARS-CoV-2 S glycoprotein, we evaluated the ability of p
264 al dispersal and increasing frequency of the SARS-CoV-2 spike protein variant D614G are suggestive of
265 nt of guidance to reduce transmission of the SARS-CoV-2 virus, responsible for the COVID-19 pandemic.
267 ate-dependent epidemic model to simulate the SARS-CoV-2 pandemic by probing different scenarios based
271 AIR) platform for detection of antibodies to SARS-CoV-2, SARS-CoV-1, MERS, three circulating coronavi
272 n contrast to mice, are highly permissive to SARS-CoV-2 and develop bronchopneumonia and strong infla
273 veolar type-II-like cells) are permissive to SARS-CoV-2 infection, and showed robust induction of che
274 do not know regarding our immune response to SARS-CoV-2, and provide a number of scenarios for which
275 found sex differences in immune responses to SARS-CoV-2 and the predictors of disease progression.
279 Recent studies have shown that, similarly to SARS-CoV, SARS-CoV-2 utilises the Spike glycoprotein on
284 goal of this study was to determine whether SARS-CoV-2 RNA could be detected from NP samples via a d
287 me-wide CRISPR screens in Vero-E6 cells with SARS-CoV-2, Middle East respiratory syndrome CoV (MERS-C
288 ing infection of AT2 and basal cultures with SARS-CoV-2 and identifying club cells as a target popula
289 S-CoV-2 shares many biological features with SARS-CoV, the zoonotic virus that caused the 2002 outbre
292 y and high-risk APOL1 genotype infected with SARS-CoV-2 have emerged during the COVID-19 pandemic.
293 Although the diagnosis of infection with SARS-CoV-2 is microbiological, imaging techniques play a
295 nanswered question is whether infection with SARS-CoV-2 results in protective immunity against reexpo
296 VID-19, the disease caused by infection with SARS-CoV-2, requires urgent development of therapeutic i
298 mell was more prevalent in participants with SARS-CoV-2 antibodies, compared with those without antib
299 nt it is unclear how common reinfection with SARS-CoV-2 is and how long serum antibodies and virus-sp