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10.1016/j.ijbiomac.2020.06.228

http://scihub22266oqcxt.onion/10.1016/j.ijbiomac.2020.06.228
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suck abstract from ncbi


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pmid32599245      Int+J+Biol+Macromol 2020 ; 163 (ä): 1-8
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  • Targeting hub genes and pathways of innate immune response in COVID-19: A network biology perspective #MMPMID32599245
  • Prasad K; Khatoon F; Rashid S; Ali N; AlAsmari AF; Ahmed MZ; Alqahtani AS; Alqahtani MS; Kumar V
  • Int J Biol Macromol 2020[Nov]; 163 (ä): 1-8 PMID32599245show ga
  • The current pandemic of 2019 novel coronavirus disease (COVID-19) caused by a novel virus strain, 2019-nCoV/SARS-CoV-2 have posed a serious threat to global public health and economy. It is largely unknown how the human immune system responds to this infection. A better understanding of the immune response to SARS-CoV-2 will be important to develop therapeutics against COVID-19. Here, we have used transcriptomic profile of human alveolar adenocarcinoma cells (A549) infected with SARS-CoV-2 and employed a network biology approach to generate human-virus interactome. Network topological analysis discovers 15 SARS-CoV-2 targets, which belongs to a subset of interferon (IFN) stimulated genes (ISGs). These ISGs (IFIT1, IFITM1, IRF7, ISG15, MX1, and OAS2) can be considered as potential candidates for drug targets in the treatments of COVID-19. We have identified significant interaction between ISGs and TLR3 agonists, like poly I: C, and imiquimod, and suggests that TLR3 agonists can be considered as a potential drug for drug repurposing in COVID-19. Our network centric analysis suggests that moderating the innate immune response is a valuable approach to target COVID-19.
  • |A549 Cells[MESH]
  • |Antiviral Agents/pharmacology[MESH]
  • |Betacoronavirus/*genetics/immunology[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*genetics/immunology/virology[MESH]
  • |Drug Repositioning[MESH]
  • |ELAV-Like Protein 2/*genetics/immunology/*metabolism[MESH]
  • |Gene Regulatory Networks[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Interferon-gamma/immunology/pharmacology[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*genetics/immunology/virology[MESH]
  • |Protein Interaction Maps/genetics[MESH]
  • |SARS-CoV-2[MESH]
  • |Signal Transduction[MESH]


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