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Multi-organ Dysfunction Due to SARS-CoV-2 Infection: A Comparative Overview

Received: 26 November 2020     Accepted: 15 December 2020     Published: 22 January 2021
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Abstract

SARS-CoV-2 or COVID-19 is a highly transmittable and pathogenic viral disease, which was first reported in the province Wuhan of China in late December 2019. The disease has shown its catastrophic effect in more than 200 countries and territories, causing more than 53.7 million confirmed cases and over 1.3 million deaths since its outbreak. Although the virus was primarily presumed to cause respiratory disease, reports are emerging of the plausible impact of the virus on multiple organs. The multi-organ dysfunction in severe patients of COVID-19 results in high morbidity and mortality rate compared to the other coronavirus family members like SARS and MERS. In this review, we provided a brief overview of the current insights of potential COVID-19 impacts on multiple organ functions. Reports suggest that the virus may exert direct (e.g., using ACE2 receptor) or indirect (e.g., cytokine storm) effects on several organs, including the lung, kidney, heart, liver, and brain. These multi-organ injuries may contribute to poor health outcomes and even may lead to death, especially to those suffering from cardiac disease, diabetes, liver, kidney diseases, etc. However, further investigation is required to know the exact mechanism of the infection. This study will provide valuable information on multi-organ dysfunction due to COVID-19 and thus, help clinicians to combat the disease until an effective vaccine arrives.

Published in American Journal of Internal Medicine (Volume 9, Issue 1)
DOI 10.11648/j.ajim.20210901.15
Page(s) 26-35
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2021. Published by Science Publishing Group

Keywords

SARS-CoV-2, Pandemic, Multi-Organ Failure, Angiotensin-Converting Enzyme 2 (ACE2), Cytokine Storm

References
[1] Morens D. M., Folkers G. K., and Fauci A. S. (2009). What is a pandemic? Journal of Infectious Diseases, 200: 1018–1021.
[2] Cucinotta D. and Vanelli M. (2020). WHO declares COVID-19 a pandemic. Acta Biomedica, 91: 157–160.
[3] Saghazadeh A. and Rezaei N. (2020). Immune-epidemiological parameters of the novel coronavirus–a perspective. Expert Review of Clinical Immunology, 16: 465–470.
[4] Li Q., Guan X., Wu P., Wang X., Zhou L., Tong Y., et al. (2020). Early transmission dynamics in Wuhan, China, of novel coronavirus-infected pneumonia. New England Journal of Medicine, 382: 1199–1207.
[5] Devaux C. A., Rolain J. M., and Raoult D. (2020). ACE2 receptor polymorphism: Susceptibility to SARS-CoV-2, hypertension, multi-organ failure, and COVID-19 disease outcome. Journal of Microbiology, Immunology and Infection, 53 (3): 425-435.
[6] Yuefei J., Haiyan Y., Wangquan J., Weidong W., Shuaiyin C. W. Z., and Duan G. (2020). Virology, epidemiology, pathogenesis, and control of COVID-19. Viruses, 12 (4): 372.
[7] Wang C., Horby P. W., Hayden F. G., and Gao G. F. (2020). A novel coronavirus outbreak of global health concern. The Lancet, 395: 470–473.
[8] Hu B., Guo H., Zhou P., and Shi Z. L. (2020). Characteristics of SARS-CoV-2 and COVID-19. Nature Reviews Microbiology, 1-14.
[9] Zhang Y. Z. and Holmes E. C. (2020). A genomic perspective on the origin and emergence of SARS-CoV-2. Cell, 181: 223–227.
[10] Peiris J. S. M., Guan Y., and Yuen K. Y. (2004). Severe acute respiratory syndrome. Nature Medicine, 10: S88–97.
[11] Chen L., Lou J., Bai Y., and Wang M. (2020). COVID-19 disease with positive fecal and negative pharyngeal and sputum viral tests. American Journal of Gastroenterology, 115: 790.
[12] Zou X., Chen K., Zou J., Han P., Hao J., and Han Z. (2020). Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Frontiers of Medicine, e1-8.
[13] Huang C., Wang Y., Li X., Ren L., Zhao J., Hu Y., et al. (2020). Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. The Lancet, 395: 497–506.
[14] Napoleoni L. (2005). Profile of a killer. Foreign Policy, 151: 36–43.
[15] Adhikari S. P., Meng S., Wu Y., Mao Y., Ye R., Wang Q., et al. (2020). A scoping review of 2019 novel coronavirus during the early outbreak period: Epidemiology, causes, clinical manifestation and diagnosis, prevention and control. Research Square.
[16] Hu B., Huang S., and Yin L. (2020). The cytokine storm and COVID-19. Journal of Medical Virology.
[17] Madjid M., Safavi-Naeini P., and Solomon S. D., and Vardeny O. (2020). Potential effects of coronaviruses on the cardiovascular system: A Review. JAMA Cardiology, 5: 831–840.
[18] Baig A. M., Khaleeq A., Ali U., and Syeda H. (2020). Evidence of the COVID-19 Virus targeting the CNS: tissue distribution, host-virus interaction, and proposed neurotropic mechanisms. ACS Chemical Neuroscience, 11: 995–998.
[19] Channappanavar R. and Perlman S. (2017). Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Seminars in Immunopathology, 39: 529–539.
[20] Paramasivam A., Priyadharsini J. V., Raghunandhakumar S., and Elumalai P. (2020). A novel COVID-19 and its effects on cardiovascular disease. Hypertension Research, 43: 729–730.
[21] Kumar M. P., Mishra S., Jha D. K., Shukla J., et al. (2020). Coronavirus disease (COVID-19) and the liver: a comprehensive systematic review and meta-analysis. Hepatology International, 14: 711–722.
[22] Arbour N., Day R., Newcombe J., and Talbot P. J. (2000). Neuroinvasion by human respiratory coronaviruses. Journal of Virology, 74: 8913–8921.
[23] Ioannidis J. P. A. (2020). Global perspective of COVID-19 epidemiology for a full-cycle pandemic. European journal of clinical investigation, e13421.
[24] Clark A., Jit M., Warren-Gash C., Guthrie B., et al. (2020). Global, regional, and national estimates of the population at increased risk of severe COVID-19 due to underlying health conditions in 2020: a modelling study. The Lancet Global Health, 8: 1003–1017.
[25] Burki T. (2020). China’s successful control of COVID-19. The Lancet Infectious diseases, 3099: 19–20.
[26] Petersen E., Koopmans M., Go U., Hamer D, H., et al. (2020). Comparing SARS-CoV-2 with SARS-CoV and influenza pandemics. The Lancet Infectious Diseases, 20 (9): 238-244.
[27] Randolph H. E. and Barreiro L. B. (2020). Herd immunity: understanding COVID-19. Immunity, 52: 737–741.
[28] Conti P., Ronconi G., Caraffa A., Gallenga C. E., et al. (2020). Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): anti-inflammatory strategies. Journal of biological regulators and homeostatic agents, 34: 327–331.
[29] Shi H., Han X., Jiang N., Cao Y., et al. (2020). Radiological findings from 81 patients with COVID-19 pneumonia in Wuhan, China: a descriptive study. The Lancet Infectious Diseases, 20: 425–434.
[30] Zhao W., Zhong Z., Xie X., Yu Q., and Liu J. (2020). Relation between chest CT findings and clinical conditions of coronavirus disease (covid-19) pneumonia: A multicenter study. American Journal of Roentgenology, 214: 1072–1077.
[31] Pan F., Ye T., Sun P., Gui S., et al. (2020). Time course of lung changes on chest CT during recovery from 2019 novel coronavirus (COVID-19) pneumonia. Radiology, e200370.
[32] Inui, S., Fujikawa, A., Jitsu, M., Kunishima, N., et al. (2020). Chest CT findings in cases from the cruise ship “Diamond Princess” with coronavirus disease 2019 (COVID-19). Radiology. Cardiothoracic Imaging, 2 (2): e200110.
[33] McGonagle D., O’Donnell J. S., Sharif K., Emery P., and Bridgewood C. (2020). Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia. The Lancet Rheumatology, 2: 437–445.
[34] Gattinoni L., Chiumello D., Caironi P., Busana M., et al. (2020). COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Medicine, 46: 1099–1102.
[35] Marini J. J. and Gattinoni L. (2020). Management of COVID-19 respiratory distress. Jama, 7: 435–444.
[36] Menter T., Haslbauer J. D., Nienhold R., Savic S., Hopfer H., et al. (2020). Postmortem examination of COVID-19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction. Histopathology, 77: 198–209.
[37] Carsana L., Sonzogni A., Nasr A., Rossi R. S., et al. (2020). Pulmonary post-mortem findings in a series of COVID-19 cases from northern Italy: a two-centre descriptive study. The Lancet Infectious Diseases, 20: 1135–1140.
[38] Pascarella G., Strumia A., Piliego C., Bruno F., et al. (2020). COVID-19 diagnosis and management: a comprehensive review. Journal of Internal Medicine, 288: 192–206.
[39] Chen J. Y., Qiao K., Liu F., Wu B., Xu X., et al. (2020). Lung transplantation as therapeutic option in acute respiratory distress syndrome for coronavirus disease 2019-related pulmonary fibrosis. Chinese Medical Journal, 133: 1390–6.
[40] Guzik T. J., Mohiddin S. A., Dimarco A., Patel V., Savvatis K., et al. (2020). COVID-19 and the cardiovascular system: Implications for risk assessment, diagnosis, and treatment options. Cardiovascular Research, 116: 1666–87.
[41] Lang J. P., Wang X., Moura F. A., Siddiqi H. K., Morrow D. A., and Bohula E. A. (2020). A current review of COVID-19 for the cardiovascular specialist. American Heart Journal, 226: 29–44.
[42] ALkharashi N. A. (2019). Brief communication. Saudi Medical Journal, 40: 1290–1293.
[43] Pei G., Zhang Z., Peng J., Liu L., Zhang C., Yu C., et al. (2020). Renal involvement and early prognosis in patients with COVID-19 pneumonia. Journal of the American Society of Nephrology, 31 (6): 1157-1165.
[44] Yin Y. and Wunderink R. G. (2018). MERS, SARS and other coronaviruses as causes of pneumonia. Respirology, 23 (2): 130-137.
[45] Ali N. and Mahmood S. (2020). Kidney Injury in COVID-19: an emerging concern to the clinician. SN Compr Clin Med, 2: 1808–1809.
[46] Naicker S., Yang C. W., Hwang S. J., Liu B. C., Chen J. H., and Jha V. (2020). The novel coronavirus 2019 epidemic and kidneys. Kidney International, 97 (5): 824-828.
[47] Hamming I., Timens W., Bulthuis M. L. C., Lely A. T., Navis G. J., and van Goor H. (2004). Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. Journal of Pathology, 203 (2): 631-637.
[48] Sun J., Zhu A., Li H., Zheng K., Zhuang Z., et al. (2020). Isolation of infectious SARS-CoV-2 from urine of a COVID-19 patient. Emerging Microbes and Infections, 9 (1): 991-993.
[49] Su H., Yang M., Wan C., Yi L. X., Tang F., et al. (2020). Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney International. 98 (1): 219-227.
[50] Kissling S., Rotman S., Gerber C., Halfon M., Lamoth F., et al. (2020). Collapsing glomerulopathy in a COVID-19 patient. Kidney International, 98 (1): 228–231.
[51] Santoriello D, Khairallah P, Bomback AS, Xu K, Kudose S, Batal I, et al. (2020). Postmortem kidney pathology findings in patients with COVID-19. Journal of the American Society of Nephrology, 31 (9): 2158-2167.
[52] Kudose S., Batal I., Santoriello D., Xu K., Barasch J., et al. (2020). Kidney biopsy findings in patients with COVID-19. Journal of the American Society of Nephrology, 31 (9): 1959-1968.
[53] Diao B., Wang C., Wang R., Feng Z., Tan Y., et al. (2020). Human kidney is a target for novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Infection. MedRxiv.
[54] Ding Y., He L., Zhang Q., Huang Z., Che X., Hou J., et al. (2004). Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS-CoV) in SARS patients: Implications for pathogenesis virus transmission pathways. Journal of Pathology, 203 (2): 622-630.
[55] Yeung M. L., Yao Y., Jia L., Chan J. F. W., Chan K. H., et al. (2016). MERS coronavirus induces apoptosis in kidney and lung by upregulating Smad7 and FGF2. Nature Microbiology, 1 (3): 1-8.
[56] Ronco C. and Reis T. (2020). Kidney involvement in COVID-19 and rationale for extracorporeal therapies. Nature Reviews Nephrology, 16: 308–310.
[57] Khouchlaa A. and Bouyahya A. (2020). COVID-19 nephropathy; probable mechanisms of kidney failure. Journal of Nephropathology, 9 (4): 1-4.
[58] Joannidis M., Forni L. G., Klein S. J., Honore P. M., Kashani K., et al. (2020). Lung–kidney interactions in critically ill patients: consensus report of the acute disease quality initiative (ADQI) 21 workgroup. Intensive Care Medicine, e1-19.
[59] Husain S. F., Slutsky A. S., and Ronco C. (2016). Lung-kidney cross-talk in the critically ill patient. American Journal of Respiratory and Critical Care Medicine, 194 (4): 402-414.
[60] Oussalah A., Gleye S., Clerc Urmes I., Laugel E., Callet J., et al. (2020). Long-term ACE inhibitor/ARB use is associated with severe renal dysfunction and acute kidney injury in patients with severe COVID-19: Results from a referral center cohort in the Northeast of France. Clinical Infectious Diseases, e1–10.
[61] Sabbahy M. E. and Vaidya V. S. (2011). Ischemic kidney injury and mechanisms of tissue repair. Wiley Interdisciplinary Reviews: Systems Biology and Medicine, 3 (5): 606-618.
[62] Cheng Y., Luo R., Wang K., Zhang M., Wang Z., Dong L., et al. (2020). Kidney disease is associated with in-hospital death of patients with COVID-19. Kidney International, 97 (5): 829-838.
[63] Netland J., Meyerholz D. K., Moore S., Cassell M., and Perlman S. (2008). Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of Encephalitis in mice transgenic for human ACE2. Journal of Virology, 82: 7264–7275.
[64] Alper G. (2012). Detection of coronavirus in the central nervous system of a child with acute disseminated Encephalomyelitis. Journal of Child Neurology, 27: 1408–1425.
[65] Guastalegname M. and Vallone A. (2020). Self-reported olfactory and taste disorders in patients with severe acute respiratory coronavirus 2 infection: A cross-sectional study. Clinical Infectious Diseases, 71 (15): 888–890.
[66] Mao L., Jin H., Wang M., Hu Y., Chen S., He Q., et al. (2020). Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurology, 77: 683–690.
[67] Aghagoli G., Gallo Marin B., Katchur N. J., Chaves-Sell F., Asaad W. F., and Murphy S. A. (2020). Neurological involvement in COVID-19 and potential mechanisms: A review. Neurocritical Care, e1-10.
[68] Dijkman R., Jebbink M. F., Koekkoek S. M., Deijs M., et al. (2013). Isolation and characterization of current human coronavirus strains in primary human epithelial cell cultures reveal differences in target cell tropism. Journal of Virology, 87: 6081–6090.
[69] Desforges M., Le C. A., Dubeau P., Bourgouin A., Lajoie L., Dubé M., et al. (2019). Human coronaviruses and other respiratory viruses: Underestimated opportunistic pathogens of the central nervous system? Viruses, 12: 1–28.
[70] Zubair A. S., McAlpine L. S., Gardin T., Farhadian S., Kuruvilla D. E., and Spudich S. (2020). Neuropathogenesis and neurologic manifestations of the coronaviruses in the age of coronavirus disease 2019: A review. JAMA Neurology, 77 (8): 1018-1027.
[71] Iroegbu J. D., Ifenatuoha C. W., and Ijomone O. M. (2020). Potential neurological impact of coronaviruses: implications for the novel SARS-CoV-2. Neurological Sciences, 41: 1329–1337.
[72] Gu J., Gong E., Zhang B., Zheng J., Gao Z., et al. (2005). Multiple organ infection and the pathogenesis of SARS. Journal of Experimental Medicine, 202: 415–424.
[73] Swanson P. and McGavern D. (2015). Portals of viral entry into the central nervous system. The Blood-Brain Barrier in Health and Disease, 2: 23–47.
[74] Desforges M., Miletti T. C., Gagnon M., and Talbot P. J. (2007). Activation of human monocytes after infection by human coronavirus 229E. Virus Research, 130: 228–240.
[75] Morris M. and Zohrabian V. M. (2020). Neuroradiologists, be mindful of the neuroinvasive potential of COVID-19. American Journal of Neuroradiology, 41: 37–39.
[76] Desforges M., Le C. A., Stodola J. K., Meessen-Pinard M., and Talbot P. J. (2014). Human coronaviruses: Viral and cellular factors involved in neuroinvasiveness and neuropathogenesis. Virus Research, 194: 145–158.
[77] Spiegel M., Schneider K., Weber F., Weidmann M., and Hufert F. T. (2006). Interaction of severe acute respiratory syndrome-associated coronavirus with dendritic cells. Journal of General Virology, 87: 1953–1960.
[78] Poyiadji N., Shahin G., Noujaim D., Stone M., Patel S., and Griffith B. (2020). COVID-19-associated acute hemorrhagic necrotizing encephalopathy: Imaging features. Radiology, 296: 119–120.
[79] De Haan C. A., De Wit M., Kuo, L., et al. (2003). The glycosylation status of the murine hepatitis coronavirus M protein affects the interferogenic capacity of the virus in vitro and its ability to replicate in the liver but not the brain. Virology, 312 (2): 395–406.
[80] Li J., and Fan J. (2020). Characteristics and mechanism of liver injury in 2019 coronavirus disease. Journal of Clinical and Translational Hepatology, 8 (1): 13–17.
[81] Musa S. (2020). Hepatic and gastrointestinal involvement in coronavirus disease 2019 (COVID-19): What do we know till now ? Arab Journal of Gastroenterology, 21: 3–8.
[82] Ali N. and Hossain K. (2020). Liver injury in severe COVID-19 infection : current insights and challenges liver injury in severe COVID-19 infection : current insights and challenges. Expert Review of Gastroenterology & Hepatology, 14 (10): 879-884.
[83] Zhang C., Shi L., and Wang F. (2020). Liver injury in COVID-19 : management and challenges. The Lancet Gastroenterology & Hepatology, 5: 428–430.
[84] Jothimani D., Venugopal R., Abedin M. F., Kaliamoorthy I., and Rela M. (2020). COVID-19 and the liver. Journal of Hepatology, 73: 1231–1240.
[85] Ali N. (2020). Relationship between COVID-19 infection and liver injury: A review of recent data. Front Med, 7: 458.
[86] Ji D., Zhang D., Yang T., Mu J., Zhao P., Xu J., et al. (2020). Effect of COVID-19 on patients with compensated chronic liver diseases. Hepatology International, 14: 701–710.
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    Moshiul Alam Mishu, Fairoz Samiha, Kohinoor Zahan, Akash Saha, Shahida Ferdousee. (2021). Multi-organ Dysfunction Due to SARS-CoV-2 Infection: A Comparative Overview. American Journal of Internal Medicine, 9(1), 26-35. https://doi.org/10.11648/j.ajim.20210901.15

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    ACS Style

    Moshiul Alam Mishu; Fairoz Samiha; Kohinoor Zahan; Akash Saha; Shahida Ferdousee. Multi-organ Dysfunction Due to SARS-CoV-2 Infection: A Comparative Overview. Am. J. Intern. Med. 2021, 9(1), 26-35. doi: 10.11648/j.ajim.20210901.15

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    AMA Style

    Moshiul Alam Mishu, Fairoz Samiha, Kohinoor Zahan, Akash Saha, Shahida Ferdousee. Multi-organ Dysfunction Due to SARS-CoV-2 Infection: A Comparative Overview. Am J Intern Med. 2021;9(1):26-35. doi: 10.11648/j.ajim.20210901.15

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  • @article{10.11648/j.ajim.20210901.15,
      author = {Moshiul Alam Mishu and Fairoz Samiha and Kohinoor Zahan and Akash Saha and Shahida Ferdousee},
      title = {Multi-organ Dysfunction Due to SARS-CoV-2 Infection: A Comparative Overview},
      journal = {American Journal of Internal Medicine},
      volume = {9},
      number = {1},
      pages = {26-35},
      doi = {10.11648/j.ajim.20210901.15},
      url = {https://doi.org/10.11648/j.ajim.20210901.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20210901.15},
      abstract = {SARS-CoV-2 or COVID-19 is a highly transmittable and pathogenic viral disease, which was first reported in the province Wuhan of China in late December 2019. The disease has shown its catastrophic effect in more than 200 countries and territories, causing more than 53.7 million confirmed cases and over 1.3 million deaths since its outbreak. Although the virus was primarily presumed to cause respiratory disease, reports are emerging of the plausible impact of the virus on multiple organs. The multi-organ dysfunction in severe patients of COVID-19 results in high morbidity and mortality rate compared to the other coronavirus family members like SARS and MERS. In this review, we provided a brief overview of the current insights of potential COVID-19 impacts on multiple organ functions. Reports suggest that the virus may exert direct (e.g., using ACE2 receptor) or indirect (e.g., cytokine storm) effects on several organs, including the lung, kidney, heart, liver, and brain. These multi-organ injuries may contribute to poor health outcomes and even may lead to death, especially to those suffering from cardiac disease, diabetes, liver, kidney diseases, etc. However, further investigation is required to know the exact mechanism of the infection. This study will provide valuable information on multi-organ dysfunction due to COVID-19 and thus, help clinicians to combat the disease until an effective vaccine arrives.},
     year = {2021}
    }
    

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    AU  - Moshiul Alam Mishu
    AU  - Fairoz Samiha
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    JF  - American Journal of Internal Medicine
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    AB  - SARS-CoV-2 or COVID-19 is a highly transmittable and pathogenic viral disease, which was first reported in the province Wuhan of China in late December 2019. The disease has shown its catastrophic effect in more than 200 countries and territories, causing more than 53.7 million confirmed cases and over 1.3 million deaths since its outbreak. Although the virus was primarily presumed to cause respiratory disease, reports are emerging of the plausible impact of the virus on multiple organs. The multi-organ dysfunction in severe patients of COVID-19 results in high morbidity and mortality rate compared to the other coronavirus family members like SARS and MERS. In this review, we provided a brief overview of the current insights of potential COVID-19 impacts on multiple organ functions. Reports suggest that the virus may exert direct (e.g., using ACE2 receptor) or indirect (e.g., cytokine storm) effects on several organs, including the lung, kidney, heart, liver, and brain. These multi-organ injuries may contribute to poor health outcomes and even may lead to death, especially to those suffering from cardiac disease, diabetes, liver, kidney diseases, etc. However, further investigation is required to know the exact mechanism of the infection. This study will provide valuable information on multi-organ dysfunction due to COVID-19 and thus, help clinicians to combat the disease until an effective vaccine arrives.
    VL  - 9
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Author Information
  • Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, Bangladesh

  • Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, Bangladesh

  • Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, Bangladesh

  • Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, Bangladesh

  • Department of Biochemistry and Molecular Biology, Shahjalal University of Science and Technology, Sylhet, Bangladesh

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