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10.1007/s12250-020-00207-4

http://scihub22266oqcxt.onion/10.1007/s12250-020-00207-4
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32125642!7090474!32125642
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suck abstract from ncbi


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pmid32125642      Virol+Sin 2020 ; 35 (3): 266-271
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  • Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools #MMPMID32125642
  • Fu Y; Cheng Y; Wu Y
  • Virol Sin 2020[Jun]; 35 (3): 266-271 PMID32125642show ga
  • Currently there is no effective antiviral therapy for SARS-CoV-2 infection, which frequently leads to fatal inflammatory responses and acute lung injury. Here, we discuss the various mechanisms of SARS-CoV-mediated inflammation. We also assume that SARS-CoV-2 likely shares similar inflammatory responses. Potential therapeutic tools to reduce SARS-CoV-2-induced inflammatory responses include various methods to block FcR activation. In the absence of a proven clinical FcR blocker, the use of intravenous immunoglobulin to block FcR activation may be a viable option for the urgent treatment of pulmonary inflammation to prevent severe lung injury. Such treatment may also be combined with systemic anti-inflammatory drugs or corticosteroids. However, these strategies, as proposed here, remain to be clinically tested for effectiveness.
  • |Acute Lung Injury/immunology/virology[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Animals[MESH]
  • |Anti-Inflammatory Agents/*therapeutic use[MESH]
  • |Antibodies, Viral[MESH]
  • |Antibody-Dependent Enhancement/immunology[MESH]
  • |Betacoronavirus/immunology/pathogenicity[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*drug therapy/*immunology[MESH]
  • |Cytokines/metabolism[MESH]
  • |Humans[MESH]
  • |Inflammation/*drug therapy/immunology[MESH]
  • |Lung/immunology[MESH]
  • |Pandemics[MESH]
  • |Peptidyl-Dipeptidase A/metabolism[MESH]
  • |Pneumonia, Viral/*drug therapy/*immunology[MESH]
  • |SARS-CoV-2[MESH]
  • |Spike Glycoprotein, Coronavirus/immunology[MESH]


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