期刊
VIROLOGICA SINICA
卷 35, 期 3, 页码 266-271出版社
KEAI PUBLISHING LTD
DOI: 10.1007/s12250-020-00207-4
关键词
SARS-CoV-2; Inflammatory response; Fc receptors (FcR); Antibody-dependent enhancement (ADE)
类别
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.
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