LitCovid-sentences  

PMC:7736111 / 22442-26353 JSONTXT 2 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function

Id Subject Object Predicate Lexical cue
T128 0-74 Sentence denotes Inhibition of Host Cell Biosynthetic Pathways and Modulation of Cell Death
T129 75-179 Sentence denotes Both SARS-CoV and SARS-CoV-2 have evolved multiple inhibitory mechanisms to evade host cell recognition.
T130 180-339 Sentence denotes Inhibition of host transcriptional and translational machinery prevents the biosynthesis of protective IFNs and delays early activation of host cell apoptosis.
T131 340-444 Sentence denotes Nsp1 of SARS-CoV inhibit the loading of ribosomal 40s subunit and prevent host cell protein translation.
T132 445-589 Sentence denotes Further, Nsp1 specifically degrade host cell RNA while sparing the viral RNA (Huang et al., 2011; Tanaka et al., 2012; Lokugamage et al., 2015).
T133 590-693 Sentence denotes N protein of SARS-CoV-2 also interacts with the host biosynthetic protein La-related protein 1 (LARP1).
T134 694-846 Sentence denotes This interaction may serve as the necessary signal to shut down the host cell protein synthesis for the propagation of SARS-CoV-2 (Gordon et al., 2020).
T135 847-1069 Sentence denotes Papain-like protease of SARS-CoV directly interacts with p53 and induce its degradation, which may thus interfere with translation and delay early apoptosis of the infected cells (Yuan et al., 2015; Ma-Lauer et al., 2016).
T136 1070-1236 Sentence denotes SARS-CoV S protein also interacts with the translation initiation factor eIF3f and inhibit host cell translation by preventing its nuclear import (Xiao et al., 2008).
T137 1237-1476 Sentence denotes Studies from other respiratory viruses have shown that cells which activate early apoptosis prevent further spread of the viruses, whereas viruses that successfully inhibit this pathway exhibit strong infectivity (Orzalli and Kagan, 2017).
T138 1477-1668 Sentence denotes Cytomegaloviruses (CMVs) distinctly rely on this mechanism to successfully replicate within the host cell by inhibiting apoptosis-modulatory proteins such as Bax and Bcl-2 (Çam et al., 2010).
T139 1669-1895 Sentence denotes However, whether SARS-CoV or SARS-CoV-2 are also directly involved in inhibiting early apoptosis remains to be tested, but it is evident that these viruses induce host cell death after successful propagation and dissemination.
T140 1896-2022 Sentence denotes SARS-CoV Nsp7a was shown to interact with prosurvival protein Bcl-X and induce apoptosis in cells in vitro (Tan et al., 2007).
T141 2023-2156 Sentence denotes Similarly, ORF3a leads to fragmentation of the Golgi apparatus, and induction of apoptosis (Waye et al., 2005; Freundt et al., 2010).
T142 2157-2305 Sentence denotes Besides this, ORF3a also implicates necroptotic cell death by interacting with and activating the main necroptosis protein RIPK3 (Yue et al., 2018).
T143 2306-2406 Sentence denotes Owing to its role in cell death pathways, the ORF3a of SARS-CoV-2 was also explored in this context.
T144 2407-2529 Sentence denotes This protein similarly induced apoptosis in HEK293 cells by activating the caspase 8-dependent pathway (Ren et al., 2020).
T145 2530-2763 Sentence denotes Interestingly, the results, that ORF3a of SARS-CoV-2 induces relatively lower apoptosis in several cell lines as compared to SARS-CoV, suggesting that this mechanism could provide an early advantage for the propagation of SARS-CoV-2.
T146 2764-2984 Sentence denotes Further, the proteome map of SARS-CoV-2 predicted interaction of Nsp12 with RIPK1, suggesting that this viral protein may also implicate in regulating host cell apoptotic and necroptotic cell death (Gordon et al., 2020).
T147 2985-3254 Sentence denotes However, a study on 25 cell lines in culture showed SARS-CoV-2 exhibiting cytopathic effect on only two cells, indicating that the differences could exist between these two related viruses in their property to interfere with host cell death pathways (Chu et al., 2020).
T148 3255-3444 Sentence denotes Thus, more comprehensive studies are needed to provide better molecular insights by which SARS-CoV-2 modulates host cell death pathways, which may also open new opportunities for treatment.
T149 3445-3713 Sentence denotes Based on these early observations, it is becoming evident that SARS-CoV-2 interferes with host NAS, IFN, biosynthetic, and cell death pathways to prevent early immune response and thus contribute to the underlying immunopathogenesis, as will be discussed subsequently.
T150 3714-3911 Sentence denotes To make these details simple, here we compiled the role of various SARS-CoV and SARS-CoV-2 proteins and their host cell interacting proteins and presented in the Table form (Supplementary Table 1).