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10.1186/s12967-020-02405-w

http://scihub22266oqcxt.onion/10.1186/s12967-020-02405-w
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32522207!7286221!32522207
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suck abstract from ncbi


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pmid32522207      J+Transl+Med 2020 ; 18 (1): 233
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  • COVID-19: viral-host interactome analyzed by network based-approach model to study pathogenesis of SARS-CoV-2 infection #MMPMID32522207
  • Messina F; Giombini E; Agrati C; Vairo F; Ascoli Bartoli T; Al Moghazi S; Piacentini M; Locatelli F; Kobinger G; Maeurer M; Zumla A; Capobianchi MR; Lauria FN; Ippolito G
  • J Transl Med 2020[Jun]; 18 (1): 233 PMID32522207show ga
  • BACKGROUND: Epidemiological, virological and pathogenetic characteristics of SARS-CoV-2 infection are under evaluation. A better understanding of the pathophysiology associated with COVID-19 is crucial to improve treatment modalities and to develop effective prevention strategies. Transcriptomic and proteomic data on the host response against SARS-CoV-2 still have anecdotic character; currently available data from other coronavirus infections are therefore a key source of information. METHODS: We investigated selected molecular aspects of three human coronavirus (HCoV) infections, namely SARS-CoV, MERS-CoV and HCoV-229E, through a network based-approach. A functional analysis of HCoV-host interactome was carried out in order to provide a theoretic host-pathogen interaction model for HCoV infections and in order to translate the results in prediction for SARS-CoV-2 pathogenesis. The 3D model of S-glycoprotein of SARS-CoV-2 was compared to the structure of the corresponding SARS-CoV, HCoV-229E and MERS-CoV S-glycoprotein. SARS-CoV, MERS-CoV, HCoV-229E and the host interactome were inferred through published protein-protein interactions (PPI) as well as gene co-expression, triggered by HCoV S-glycoprotein in host cells. RESULTS: Although the amino acid sequences of the S-glycoprotein were found to be different between the various HCoV, the structures showed high similarity, but the best 3D structural overlap shared by SARS-CoV and SARS-CoV-2, consistent with the shared ACE2 predicted receptor. The host interactome, linked to the S-glycoprotein of SARS-CoV and MERS-CoV, mainly highlighted innate immunity pathway components, such as Toll Like receptors, cytokines and chemokines. CONCLUSIONS: In this paper, we developed a network-based model with the aim to define molecular aspects of pathogenic phenotypes in HCoV infections. The resulting pattern may facilitate the process of structure-guided pharmaceutical and diagnostic research with the prospect to identify potential new biological targets.
  • |*Gene Regulatory Networks[MESH]
  • |*Host-Pathogen Interactions[MESH]
  • |*Models, Biological[MESH]
  • |*Protein Interaction Mapping[MESH]
  • |Betacoronavirus/*physiology[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*genetics/*virology[MESH]
  • |Humans[MESH]
  • |Membrane Glycoproteins/metabolism[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*genetics/*virology[MESH]
  • |SARS-CoV-2[MESH]
  • |Signal Transduction/genetics[MESH]


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