China
Africa
Explore chapters and articles related to this topic
COVID-19 pathogenesis and host immune response
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Surbhi Bihani, Shalini Aggarwal, Arup Acharjee
Gordon et al. sought to characterize the host–virus protein–protein interactions (PPIs) to lay the groundwork for dissecting the exact molecular mechanism of viral pathogenesis (Gordon et al. 2020). The virus undertakes the deception in two crucial acts. Suppression of immune response is act one. The induction of IFN-I is critical for the innate immune response against viral infections (Stetson and Medzhitov 2006). Using biotin-streptavidin affinity purification mass spec-trometry (AP-MS), it was found that Orf9b of SARS-CoV-2 localizes on the outer membrane of host cell mitochondrial protein TOM70 to suppress type I interferon (IFN-I) responses (Jiang, Zhang et al. 2020). Further viral proteins ORF6, ORF8, and nucleocapsid also inhibit IFN-I signaling allowing immune evasion (Flower et al. 2021; J.-Y. Li et al. 2020). Moreover, the non-structural protein-1 has been shown to interact with the 40S ribosomal subunit to inhibit the mRNA synthesis of the retinoic acid–inducible gene I-dependent innate immune responses. Therefore, it could entirely block the translation of IFNs and IFN-stimulated genes (ISGs) that usually facilitate viral clearance (Thoms et al. 2020). The upregulation of inflammatory response synergistically complements the inhibition of interferon response.
New strategies for treatment of COVID-19 and evolution of SARS-CoV-2 according to biodiversity and evolution theory
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Fortunately, mutations in the genome region of the virus’s spikes may weaken the virus’s attachment to its receptors in the host cell. This may explain the extent of the variation in the severity of the response between people each other and between different countries of this disease (COVID-19). Interactions between the SARS-CoV spike protein receptor-binding domain (RBD) and its host receptor angiotensin-converting enzyme 2 (ACE2) regulate both the cross-species and human-to-human transmissions of SARS-CoV. The sequence of 2019-nCoV RBD, including its receptor-binding motif (RBM) that directly contacts ACE2, is similar to that of SARS-CoV, strongly suggesting that 2019-nCoV uses ACE2 as its receptor [37]. The crystal structure of the C-terminal domain of SARS-CoV-2 (SARS-CoV-2-CTD) spike (S) protein was demonstrated, in complex with human ACE2 (hACE2), which reveals a hACE2-binding mode similar overall to that observed for SARS-CoV. These findings shed light on the viral pathogenesis and provide important structural information regarding development of therapeutic countermeasures against the emerging virus [38].