In December 2019, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), a novel variant of coronavirus has recently emerged from Wuhan in China and has created havoc impulses across the world for a larger number of fatalities. At the same time studies are going on to discover vaccine against it or repurposing of approved drugs is widely adopted are under trial to eradicate the SARS-CoV-2 causing COVID-19. Reports have also shown that there are asymptomatic carriers of COVID-19 disease who can transmit the disease to others too. But the first line defense of the viral attack is body’s strong and well-coordinated immune response producing excessive inflammatory innate reaction and impaired adaptive host immune defense may leading death upon the misfunctioning. Considerable works are going on to establish the relation between immune parameters and viral entry that might alter both the innate and adaptive immune system COVID patient by up riding a massive cytokines and chemokines secretion. This review mainly gives an account on how SARS-CoV-2 interact with our immune system and how does our immune system respond to it and along with that drugs which are being used or can be used in fighting the disease and curative therapies as treatment for it has also been addressed. Graphical abstract Unlabelled Image
【저자키워드】 SARS-CoV-2, immune response, COVID-19 therapy, N, nucleocapsid, S, spike, HCoV, human coronavirus, RBD, receptor binding domain, IFN, interferon, ARDS, acute respiratory distress syndrome, IL, interleukin, MIP, macrophage inflammatory protein, MERS, Middle East respiratory syndrome, RBM, receptor binding motif, PCR, polymerase chain reaction, ACE, Angiotensin converting enzyme, MSCs, mesenchymal stem cells, RA, Rheumatoid arthritis, TMPRSS2, Transmembrane Protease Serine 2, NK cells, Natural Killer cells, PAMPs, Pathogen Associated Molecular Patterns, PRRs, Pattern Recognition Receptors, E, Envelope, NAbs, neutralizing antibodies, M, membrane, ORFs, open reading frames, MHC, major histocompatibility complex, Ig, immunoglobulin, CD, cluster of differentiation, MAbs, monoclonal antibodies, BAL, bronchoalveolar lavage, SLE, systemic lupus erythematosus, IRF, Interferon regulatory factor, STAT, Signal transducer and activator of transcription, FGF, fibroblast growth factor, PDGF, platelet derived growth factor, G-CSF, Granulocyte colony stimulating factor, Myd88, Myeloid differentiation primary response 88, DPP4, dipeptidyl peptidase 4, nsps, Non-structural proteins, Agn, angiotensin, AMs, alveolar macrophages, APCs, antigen presenting cells, ASCs, antigen secreting cells, AT2, alveolar type 2, cDCs, conventional dendritic cells, CCL, C-C motif chemokine ligand, CDHR3, cadherin related family member 3, CLpro, chymotrypsin-like protease, Covid-19, coronavirus disease, 2019, CTL, cytotoxic T lymphocyte, CTLA, cytotoxic T lymphocyte associated antigen, CXCL, C-X-C motif chemokine ligand, CXCR, C-X-C motif chemokine receptor, DMVs, double membrane vesicles, dsDNA, double stranded DNA, dsRNA, double stranded RNA, GM-CSF, granulocyte-monocyte colony stimulating factor, GZMA, granzyme, H, hydrogen, HLA, human leucocyte antigen, ICIs, immune checkpoint inhibitors, IMs, inflammatory monocytes, IMMs, inflammatory monocyte-macrophages;IP-10, inducible protein 10, ISG, interferon stimulated gene, LAG3, lymphocyte activation gene 3, MBL, mannose binding lectin, MCP1, membrane cofactor protein 1, moDCs, monocytes-derived dendritic cells, NGS, of next generation sequencing, NKG2A, NK group 2 member 2A, PD1, programmed cell death protein 1, PD-L1, programmed cell death protein ligand 1, PLpro, papain like protease, Pp, polypeptides, RLRs, RIG-I like receptors, RTC, replication transcription complex;, SARS-CoV-2, severe acute respiratory syndrome- coronavirus-2, scRNAseq, single cell RNA sequencing, ssRNA, single stranded RNA, TIGIT, T cell immunoreceptor with Ig and ITIM domains, TIM 3, T cell immunoglobulin and mucin domain 3, TLRs, Toll like receptors, TNF, tumor necrosis factor;, VEGF A, vascular endothelial growth factor A,