PMC:7558233 / 6318-13194 JSONTXT 5 Projects

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Id Subject Object Predicate Lexical cue
T34 0-49 Sentence denotes 3 Possible mechanisms underlying viral infection
T35 50-240 Sentence denotes SARS-CoV-2 was initially identified and isolated from a cluster of patients with similar symptoms (fever, cough, and dyspnea) and radiologic findings of ground-glass opacity on chest CT [6].
T36 241-480 Sentence denotes Next-generation sequencing and real-time reverse transcription polymerase chain reaction (RT-PCR) targeting to a consensus RNA-dependent RNA polymerase (RdRp) region of panβ-CoV demonstrated the pathogen to be a novel beta coronavirus [7].
T37 481-626 Sentence denotes Electron microscopy revealed the solar appearance of virion particles, whose morphology was consistent with that of the Coronaviridae family [7].
T38 627-805 Sentence denotes SARS-CoV-2 most likely originated from bats due to its substantially high homology (96% nucleotide sequence identity) with SARS-like bat coronaviruses (BatCoV RaTG13) [11], [12].
T39 806-959 Sentence denotes A possible mechanism of the emergence of SARS-CoV-2 is that the accumulative mutations in its genome enabled the virus to cross the animal–human barrier.
T40 960-1065 Sentence denotes However, animal-to-human transmission is unlikely to have been the main driver for the COVID-19 pandemic.
T41 1066-1165 Sentence denotes SARS-CoV-2 employs mechanisms similar to those of SARS-CoV for receptor recognition and cell entry.
T42 1166-1366 Sentence denotes The spike (S) protein on the virion surface facilitates the entry of the virus into the target cells by attachment to its cognate receptor, angiotensin-converting enzyme 2 (ACE2), on the cell surface.
T43 1367-1559 Sentence denotes Transmembrane serine proteases of the target cells, such as FURIN or transmembrane protease serine 2 (TMPRSS2), induce cleavage of the S protein before membrane fusion for cellular entry [13].
T44 1560-1661 Sentence denotes Therefore, cells that co-express ACE2 and serine protease could be the primary targets of SARS-CoV-2.
T45 1662-2004 Sentence denotes Single-cell RNA-sequencing studies have also confirmed the expression of ACE2 and TMPRSS2 in a vast array of cells, including lung alveolar epithelial type II cells, nasal goblet cells, cholangiocytes, colonocytes, esophageal keratinocytes, gastrointestinal epithelial cells, pancreatic β-cells, and renal proximal tubules and podocytes [14].
T46 2005-2131 Sentence denotes These observations have provided probable explanations for multiple-organ infection and injury via direct viral tissue damage.
T47 2132-2374 Sentence denotes Moreover, clinical observations have demonstrated extrapulmonary manifestations, ranging from hematologic, cardiovascular, renal, gastrointestinal and hepatobiliary, endocrinologic, neurologic, and ophthalmologic to dermatologic systems [14].
T48 2375-2574 Sentence denotes SARS-CoV-2 attacks the host through direct tissue damage, endothelial cell damage and thrombosis, dysregulation of the immune response, and disorders of the renin-angiotensin-aldosterone system [15].
T49 2575-2756 Sentence denotes COVID-19 infection is accompanied by an aggressive inflammatory response with the release of massive pro-inflammatory cytokines in an event known as the “cytokine storm” [16], [17].
T50 2757-3438 Sentence denotes Plasma collected from COVID-19 patients with pneumonia has shown markedly increased concentrations of pro-inflammatory cytokines (interleukin-1β (IL-1β), interleukin-1 receptor antagonist (IL-1RA), IL-7, IL-8, IL-9, IL-10, fibroblast growth factor, granulocyte colony stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ), interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1α), macrophage inflammatory protein-1 beta (MIP-1β), platelet-derived growth factor (PDGF), tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor (VEGF)) [18].
T51 3439-3626 Sentence denotes Critical illness in patients has also been associated with an elevated level of IL-2, IL-7, IL-10, G-CSF, IP10, MCP-1, MIP-1α, and TNF-α plasma concentrations as compared with mild cases.
T52 3627-3928 Sentence denotes These events drive the recruitment of immune cells such as macrophages, neutrophils, and T cells into the sites of infection, causing destabilization of endothelial cell to cell and the vascular barrier and diffusing alveolar damage, and ultimately leading to multi-organ failure and subsequent death.
T53 3929-3983 Sentence denotes ACE2 is the key determinant of viral transmissibility.
T54 3984-4264 Sentence denotes Recent studies have demonstrated that the receptor binding domain of the S protein from SARS-CoV-2 displays a 10- to 20-fold higher binding capacity with ACE2 compared with that of SARS-CoV [19], [20], which may partially explain the increased transmissibility of SARS-CoV-2 [21].
T55 4265-4482 Sentence denotes SARS-CoV-2 shows a gradient of reduced infectivity from the proximal to distal respiratory tract, which coincides with the finding of progressively decreased expression of ACE2 from the oropharynx to the alveoli [22].
T56 4483-4678 Sentence denotes SARS-CoV-2 infection might be initiated from the nasal passages, followed by the aspiration of virions seeding along the respiratory tract to the lungs, rather than causing direct lung infection.
T57 4679-4936 Sentence denotes A more possible process might involve high loads of virus shedding from the initially infected respiratory tract, along with the secretion of mucus accumulating at the oropharynx cavity, and finally arriving at the tracheobronchial tree via aspiration [23].
T58 4937-5138 Sentence denotes Molecular dynamics simulations suggest that SARS-CoV-2 has a distinct binding interface to ACE2, with higher affinities and a different network of residue-residue contacts than other coronaviruses [2].
T59 5139-5239 Sentence denotes SARS-CoV-2 has a larger contact area than SARS-CoV with more conserved residues for ACE2 attachment.
T60 5240-5497 Sentence denotes Unlike coronaviruses with low pathogenicity, SARS-CoV-2 exhibits enhancement of the nuclear localization signals in the nucleocapsid protein and distinct inserts in the spike glycoprotein, which appear to be associated with the high case-fatality rate [24].
T61 5498-5623 Sentence denotes SARS-CoV-2 could evolve into diverse lineages with different magnitudes of virulence and transmissibility via mutations [25].
T62 5624-5887 Sentence denotes Several studies have documented a SARS-CoV-2 variant, aspartic acid (D) with substitution of glycine (G) at codon 614 in the S protein [25], [26], [27], [28], which is located on a B-cell epitope with a highly immunodominant region on the receptor binding domain.
T63 5888-6006 Sentence denotes An in vitro study suggested that a D614G pseudotype variant was nine times more infectious than the D614 strains [29].
T64 6007-6216 Sentence denotes Strains carrying this mutation have become dominant since December 2019, and have been frequently observed in European countries (e.g., the Netherlands, Switzerland, and France) but not as frequently in China.
T65 6217-6353 Sentence denotes Strikingly, the variant S-D614G distinguishes the SARS-CoV-2 strains that may have caused fatal infections in European populations [27].
T66 6354-6676 Sentence denotes A study on the alignment of 10 022 SARS-CoV-2 genomes from infected persons in 68 countries identified 6294 samples carrying the D614G mutation; almost all of these genomes also had another co-mutation in the proteins responsible for replication (ORF1ab P4715L; RdRp P323L) that might affect the speed of replication [28].
T67 6677-6876 Sentence denotes D614G was predicted to fine-tune the spike conformation and result in a loss of immunogenicity for B-cell recognition, a dominated process to stimulate adaptive immunity against SARS-CoV-2 infection.