Perspective of molecular immune response of SARS-COV-2 infection

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Martina Kurnia Rohmah Arif Rahman Nurdianto

Abstract

COVID-19 is a type of Pneumonia caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). When COVID-19 arise in Wuhan China and rapidly spread throughout to the World, we need to learn how pathogenesis and immune responses occur in the bodies in more detail. COVID-19 is the third Severe Respiratory Disease outbreak caused by the Coronavirus in the past two decades after Severe Acute Respiratory Syndrome (SARS) in the 2002 and Middle East Respiratory Syndrome (MERS) in 2012. The Articles from PUBMED and Research Gate were searched for studies on the immune response of COVID-19 infection by SARS-CoV-2. SARS-CoV-2 increases the number of neutrophils, suppresses IFN, increases the activity of Th1/Th17, B cells, CD8+ and CD4+, and causes cytokine storms especially pro-inflammatory cytokines which can increase respiration disorders and multi-organ damage. This review tries to explain about pathogenesis and immune responses of COVID-19 to provide a reference in designing the appropriate immune intervention for treatment and therapeutic such as drug or vaccine based on the recent research progress SARS-CoV-2 and previous studies about SARS CoV and MERS CoV.

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Rohmah, M., & Rahman Nurdianto, A. (2020). Perspective of molecular immune response of SARS-COV-2 infection. Jurnal Teknologi Laboratorium, 9(1), 58-66. https://doi.org/https://doi.org/10.29238/teknolabjournal.v9i1.218
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References

1. Lu H, Stratton CW, Tang YW. Outbreak of pneumonia of unknown etiology in Wuhan, China: The mystery and the miracle. J Med Virol. 2020;92(4):401-402. doi:10.1002/jmv.25678
2. World Health Organization. Novel Coronavirus (2019-NCoV) Situation Report - 12. World; 2020. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200201-sitrep-12-ncov.pdf?sfvrsn=273c5d35_2.
3. Bassetti M, Vena A, Giacobbe DR. The novel Chinese coronavirus (2019-nCoV) infections: Challenges for fighting the storm. Eur J Clin Invest. 2020;50(13209):1-4. doi:10.1111/eci.13209
4. World Health Organization. Coronavirus Disease 2019 (COVID-19) Situation Report - 70. World; 2020. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200330-sitrep-70-covid-19.pdf?sfvrsn=7e0fe3f8_4.
5. Kementerian Kesehatan Repulik Indonesia. Situasi COVID-19. Indonesia; 2020. https://www.kemkes.go.id/.
6. Li Q, Guan X, Wu P, et al. Early transmission dynamics in Wuhan, China, of novel coronavirus-infected pneumonia. N Engl J Med. 2020;382(13):1199-1207. doi:10.1056/NEJMoa2001316
7. Wang W, Tang J, Wei F. Updated understanding of the outbreak of 2019 novel coronavirus (2019-nCoV) in Wuhan, China. J Med Virol. 2020;92(4):441-447. doi:10.1002/jmv.25689
8. Liu J, Wu P, Gao F, et al. Novel immunodominant peptide presentation strategy: a featured HLA-A*2402-restricted cytotoxic T-lymphocyte epitope stabilized by intrachain hydrogen bonds from severe acute respiratory syndrome coronavirus nucleocapsid protein. J Virol. 2010;84(22):11849-11857. doi:10.1128/jvi.01464-10
9. Keicho N, Itoyama S, Kashiwase K, et al. Association of human leukocyte antigen class II alleles with severe acute respiratory syndrome in the Vietnamese population. Hum Immunol. 2009;70(7):527-531. doi:10.1016/j.humimm.2009.05.006
10. Chen YMA, Liang SY, Shih YP, et al. Epidemiological and genetic correlates of severe acute respiratory syndrome coronavirus infection in the hospital with the highest nosocomial infection rate in Taiwan in 2003. J Clin Microbiol. 2006;44(2):359-365. doi:10.1128/JCM.44.2.359-365.2006
11. Wang S-F, Chen K-H, Chen M, et al. Human-leukocyte antigen class I CW 1502 and class II DR 0301 genotypes are associated with resistance to severe acute respiratory syndrome (SARS) infection. Viral Immunol. 2011;24(5). doi:10.1089/vim.2011.0024
12. Tang F, Quan Y, Xin Z-T, et al. Lack of peripheral memory B cell responses in recovered patients with severe acute respiratory syndrome: a six-year follow-up study. J Immunol. 2011;186(12):7264-7268. doi:10.4049/jimmunol.0903490
13. Hajeer AH, Balkhy H, Johani S, Yousef MZ, Arabi Y. Association of human leukocyte antigen class II alleles with severe Middle East respiratory syndrome-coronavirus infection. Ann Thorac Med. 2016;11(3):211-213. doi:10.4103/1817-1737.185756
14. Tu X, Chong WP, Zhai Y, et al. Functional polymorphisms of the CCL2 and MBL genes cumulatively increase susceptibility to severe acute respiratory syndrome coronavirus infection. J Infect. 2020;71(1):101-109. doi:10.1016/j.jinf.2015.03.006
15. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: lessons learned from SARS and MERS epidemic. Asian Pacific J Allergy Immunol. 2020. doi:10.12932/AP-200220-0772
16. Li G, Fan Y, Lai Y, et al. Coronavirus infections and immune responses. J Med Virol. 2020;92(4):424-432. doi:10.1002/jmv.25685
17. Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med. 2020;8(4):420-422. doi:10.1016/S2213-2600(20)30076-X
18. Su S, Wong G, Liu J, et al. Epidemiology, genetic recombination, and pathogenesis of coronaviruses. Trend Microbiol. 2016;24(6):490-502. doi:10.1016/j.tim.2016.03.003
19. Guan W, Ni Z, Hu Y, et al. Clinical characteristics of 2019 novel coronavirus infection in China. N Engl J Med. 2020;382:1708-1720. doi:10.1056/NEJMoa2002032
20. Doremalen N van, Bushmaker T, Morris DH, et al. Aerosol and surface stability of SARS-CoV-2 as compared with SARS-CoV-1. N Engl J Med. 2020;382:1564-1567. doi:10.1056/NEJMc2004973
21. Hu Z, Song C, Xu C, et al. Clinical characteristics of 24 asymptomatic infections with COVID-19 screened among close contacts in Nanjing, China. Sci China Life Sci. 2020;63(5):706-711. doi:10.1007/s11427-020-1661-4
22. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506. doi:10.1016/ S0140-6736(20)30183-5
23. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-1062. doi:10.1016/ S0140-6736(20)30566-3
24. De Wit E, Van Doremalen N, Falzarano D, Munster VJ. SARS and MERS: recent insights into emerging coronaviruses. Nat Rev Microbiol. 2016;14(8):523-534. doi:10.1038/nrmicro.2016.81
25. Jeffers SA, Tusell SM, Gillim-Ross L, et al. CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus. Proc Natl Acad Sci U S A. 2004;101(44):15748-15753. doi:10.1073/pnas.0403812101
26. Raj VS, Mou H, Smits SL, et al. Dipeptidyl peptidase 4 is a functional receptor for the emerging human coronavirus-EMC. Nature. 2013;495(7440):251-254. doi:10.1038/nature12005
27. Simmons G, Reeves JD, Rennekamp AJ, Amberg SM, Piefer AJ, Bates P. Characterization of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) spike glycoprotein-mediated viral entry. Proc Natl Acad Sci U S A. 2004;101(12):4240-4245. doi:10.1073/pnas.0306446101
28. Belouzard S, Chu VC, Whittaker GR. Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. Proc Natl Acad Sci U S A. 2009;106(14):5871-5876. doi:10.1073/pnas.0809524106
29. Mille JK, Whittaker GR. Host cell entry of Middle East respiratory syndrome coronavirus after two-step, furin-mediated activation of the spike protein. Proc Natl Acad Sci U S A. 2014;111(42):15214-15219. doi:10.1073/pnas.1407087111
30. Wang H, Yang P, Liu K, et al. SARS coronavirus entry into host cells through a novel clathrin- and caveolae-independent endocytic pathway. Cell Res. 2008;18(2):290-301. doi:10.1038/cr.2008.15
31. Kuba K, Imai Y, Ohto-Nakanishi T, Penninger JM. Trilogy of ACE2: A peptidase in the renin-angiotensin system, a SARS receptor, and a partner for amino acid transporters. Pharmacol Ther. 2010;128(1):119-128. doi:10.1016/j.pharmthera.2010.06.003
32. Fan YY, Huang ZT, Li L, et al. Characterization of SARS-CoV-specific memory T cells from recovered individuals 4 years after infection. Arch Virol. 2009;154(7):1093-1099. doi:10.1007/s00705-009-0409-6
33. Williams AE, Chambers RC. The mercurial nature of neutrophils: Still an enigma in ARDS? Am J Physiol - Lung Cell Mol Physiol. 2014;306(3):L217-L230. doi:10.1152/ajplung.00311.2013
34. Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Semin Immunopathol. 2017;39(5):529-539. doi:10.1007/s00281-017-0629-x
35. Cameron MJ, Bermejo-Martin JF, Danesh A, Muller MP, Kelvin DJ. Human immunopathogenesis of severe acute respiratory syndrome (SARS). Virus Res. 2008;133(1):13-19. doi:10.1016/j.virusres.2007.02.014
36. Min CK, Cheon S, Ha NY, et al. Comparative and kinetic analysis of viral shedding and immunological responses in MERS patients representing a broad spectrum of disease severity. Sci Rep. 2016;6:1-12. doi:10.1038/srep25359
37. Snijder EJ, van der Meer Y, Zevenhoven-Dobbe J, et al. Ultrastructure and Origin of Membrane Vesicles Associated with the Severe Acute Respiratory Syndrome Coronavirus Replication Complex. J Virol. 2006;80(12):5927-5940. doi:10.1128/jvi.02501-05
38. Channappanavar R, Fehr AR, Vijay R, et al. Dysregulated type I interferon and inflammatory monocyte-macrophage responses cause lethal pneumonia in SARS-CoV-infected mice. Cell Host Microbe. 2016;19(2):181-193. doi:10.1016/j.chom.2016.01.007
39. Channappanavar R, Fehr AR, Zheng J, et al. IFN-I response timing relative to virus replication determines MERS coronavirus infection outcomes. J Clin Invest. 2019;129(9):3625-3639. doi:10.1172/JCI126363
40. Niemeyer D, Zillinger T, Muth D, et al. Middle east respiratory syndrome coronavirus accessory protein 4a is a type I interferon antagonist. J Virol. 2013;87(22):12489-12495. doi:10.1128 /JVI.01845-13
41. Yang Y, Zhang L, Geng H, et al. The structural and accessory proteins M, ORF 4a, ORF 4b, and ORF 5 of Middle East respiratory syndrome coronavirus (MERS-CoV) are potent interferon antagonists. Protein and Cells. 2013;4:951–961. doi:10.1007/s13238-013-3096-8
42. Menachery VD, Schäfer A, Burnum-Johnson KE, et al. MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape. Proc Natl Acad Sci U S A. 2018;115(5):E1012-E1021. doi:10.1073/pnas.1706928115