Coronavirus disease 2019 (COVID-19), which is a respiratory illness associated with high mortality, has been classified as a pandemic. The major obstacles for the clinicians to contain the disease are limited information availability, difficulty in disease diagnosis, predicting disease prognosis, and lack of disease monitoring tools. Additionally, the lack of valid therapies has further contributed to the difficulties in containing the pandemic. Recent studies have reported that the dysregulation of the immune system leads to an ineffective antiviral response and promotes pathological immune response, which manifests as ARDS, myocarditis, and hepatitis. In this study, a novel platform has been described for disseminating information to physicians for the diagnosis and monitoring of patients with COVID-19. An adjuvant approach using compounds that can potentiate antiviral immune response and mitigate COVID-19-induced immune-mediated target organ damage has been presented. A prolonged beneficial effect is achieved by implementing algorithm-based individualized variability measures in the treatment regimen.
【저자키워드】 COVID-19, antiviral therapy, ARDS, coronavirus, COVID-19, Coronavirus disease 2019, Digital health, IFN, interferon, ARDS, acute respiratory distress syndrome, IL, interleukin, MCP, monocyte chemoattractant protein, SARS, Severe acute respiratory syndrome, antiviral response, MERS, Middle East respiratory syndrome, ICU, Intensive care unit, CoV, coronavirus, TNF, Tumor Necrosis Factor, Tregs, regulatory T cells, RNA, Ribonucleic acid, HLH, Hemophagocytic lymphohistiocytosis, NK cells, Natural Killer cells, RT-PCR, reverse transcriptase polymerase chain reaction, Ig, immunoglobulin, CD, cluster of differentiation, HCC, hepatocellular carcinoma, IRF, Interferon regulatory factor, RIG-I, Retinoic acid-inducible gene I, TLR, toll-like receptors, IFNβ, interferon-beta, dsRNA, double-stranded RNA, NF-κB, nuclear factor kappa-light-chain, JAK-STAT, Janus kinase signal transducer and activation of transcription, IFNR, type I IFN receptor, PRM, patterns recognition molecules, Th cells, T helper cells, APC, antigen-presenting cells, CTL, cytotoxic T cells, IP-10, IFN gamma-induced protein 10, NLR, neutrophil-lymphocyte ratio, NKT, NK T cells, S-1P, sphingosine-1-phosphate, GC, glucosylceramide, SphK, sphingosine kinase, MT, microtubules, HBC, hyperimmune bovine colostrum, HRV, heart rate variability, SK1, sphingokinase 1,