Full Text:   <2562>

Summary:  <1691>

CLC number: 

On-line Access: 2024-08-27

Received: 2023-10-17

Revision Accepted: 2024-05-08

Crosschecked: 2021-03-16

Cited: 0

Clicked: 3737

Citations:  Bibtex RefMan EndNote GB/T7714

 ORCID:

Jing ZHOU

https://orcid.org/0000-0001-6190-8053

-   Go to

Article info.
Open peer comments

Journal of Zhejiang University SCIENCE B 2021 Vol.22 No.4 P.310-317

http://doi.org/10.1631/jzus.B2000523


Structural and physiological changes of the human body upon SARS-CoV-2 infection


Author(s):  Zhonglin WU, Qi ZHANG, Guo YE, Hui ZHANG, Boon Chin HENG, Yang FEI, Bing ZHAO, Jing ZHOU

Affiliation(s):  Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cells and Regenerative Medicine, Department of Orthopedic Surgery, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China; more

Corresponding email(s):   zhoujing@zju.edu.cn

Key Words:  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Coronavirus disease 2019 (COVID-19), Pathological change, Pathogenesis


Zhonglin WU, Qi ZHANG, Guo YE, Hui ZHANG, Boon Chin HENG, Yang FEI, Bing ZHAO, Jing ZHOU. Structural and physiological changes of the human body upon SARS-CoV-2 infection[J]. Journal of Zhejiang University Science B, 2021, 22(4): 310-317.

@article{title="Structural and physiological changes of the human body upon SARS-CoV-2 infection",
author="Zhonglin WU, Qi ZHANG, Guo YE, Hui ZHANG, Boon Chin HENG, Yang FEI, Bing ZHAO, Jing ZHOU",
journal="Journal of Zhejiang University Science B",
volume="22",
number="4",
pages="310-317",
year="2021",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2000523"
}

%0 Journal Article
%T Structural and physiological changes of the human body upon SARS-CoV-2 infection
%A Zhonglin WU
%A Qi ZHANG
%A Guo YE
%A Hui ZHANG
%A Boon Chin HENG
%A Yang FEI
%A Bing ZHAO
%A Jing ZHOU
%J Journal of Zhejiang University SCIENCE B
%V 22
%N 4
%P 310-317
%@ 1673-1581
%D 2021
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2000523

TY - JOUR
T1 - Structural and physiological changes of the human body upon SARS-CoV-2 infection
A1 - Zhonglin WU
A1 - Qi ZHANG
A1 - Guo YE
A1 - Hui ZHANG
A1 - Boon Chin HENG
A1 - Yang FEI
A1 - Bing ZHAO
A1 - Jing ZHOU
J0 - Journal of Zhejiang University Science B
VL - 22
IS - 4
SP - 310
EP - 317
%@ 1673-1581
Y1 - 2021
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2000523


Abstract: 
Since December 2019, the novel coronavirus (severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)) has spread to many countries around the world, developing into a global pandemic with increasing numbers of deaths reported worldwide. To data, although some vaccines have been developed, there are no ideal drugs to treat novel coronavirus pneumonia (coronavirus disease 2019 (COVID-19)). By examining the structure of the coronavirus and briefly describing its possible pathogenesis based on recent autopsy reports conducted by various teams worldwide, this review analyzes the possible structural and functional changes of the human body upon infection with SARS-CoV-2. We observed that the most prominent pathological changes in COVID-19 patients are diffuse alveolar damage (DAD) of the lungs and microthrombus formation, resulting in an imbalance of the ventilation/perfusion ratio and respiratory failure. Although direct evidence of viral infection can also be found in other organs and tissues, the viral load is relatively small. The conclusion that the injuries of the extra-pulmonary organs are directly caused by the virus needs further investigation.

SARS-CoV-2感染对人体结构和生理的影响

概要:自2019年12月以来,新型冠状病毒(SARS-CoV-2)已蔓延至世界许多国家,目前已发展成为全球大流行,且全世界报告的死亡人数在不断增加。迄今为止,虽然已有一些疫苗研发出来,但仍没有理想的药物来治疗新型冠状病毒性肺炎(COVID-19)。本文通过对冠状病毒结构的研究,并根据世界各国最近的尸检报告简要描述其可能的发病机制,进一步分析了感染SARS-CoV-2后人体可能发生的结构和功能变化。我们观察到COVID-19患者最显著的病理改变是肺部弥漫性肺泡损伤(DAD)和微血栓形成,导致通气/灌注比失衡和呼吸衰竭。虽然在其他器官和组织中也可以发现病毒感染的直接证据,但病毒载量相对较小。肺外器官的损伤是否是由病毒直接引起的,有待进一步研究。

关键词:新型冠状病毒(SARS-CoV-2);新型冠状病毒性肺炎(COVID-19);病理改变;发病机制

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

Reference

[1]AckermannM, VerledenSE, KuehnelM, et al., 2020. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in COVID-19. N Engl J Med, 383(2):120-128.

[2]BartonLM, DuvalEJ, StrobergE, et al., 2020. COVID-19 autopsies, Oklahoma, USA. Am J Clin Pathol, 153(6):725-733.

[3]BianXW, The COVID-19 Pathology Team, 2020. Autopsy of COVID-19 patients in China. Nat Sci Rev, 7(9):1414-1418.

[4]BradleyBT, MaioliH, JohnstonR, et al., 2020. Histopathology and ultrastructural findings of fatal COVID-19 infections in Washington State: a case series. Lancet, 396(10247):320-332.

[5]BujaLM, WolfDA, ZhaoBH, et al., 2020. The emerging spectrum of cardiopulmonary pathology of the coronavirus disease 2019 (COVID-19): report of 3 autopsies from Houston, Texas, and review of autopsy findings from other United States cities. Cardiovasc Pathol, 48:107233.

[6]CastroCY, 2006. ARDS and diffuse alveolar damage: a pathologist’s perspective. Semin Thorac Cardiovasc Surg, 18(1):13-19.

[7]CatanzaroM, FagianiF, RacchiM, et al., 2020. Immune response in COVID-19: addressing a pharmacological challenge by targeting pathways triggered by SARS-CoV-2. Signal Transduct Target Ther, 5:84.

[8]Duarte-NetoAN, MonteiroRAA, da SilvaLFF, et al., 2020. Pulmonary and systemic involvement in COVID-19 patients assessed with ultrasound-guided minimally invasive autopsy. Histopathology, 77(12):186-197.

[9]DucloyerM, GaboritB, ToquetC, et al., 2020. Complete post-mortem data in a fatal case of COVID-19: clinical, radiological and pathological correlations. Int J Legal Med, 134(6):2209-2214.

[10]FehrAR, PerlmanS, 2015. Coronaviruses: an overview of their replication and pathogenesis. In: Maier HJ, Bickerton E, Britton P (Eds.), Coronaviruses: Methods and Protocols. Humana Press, New York, p.1-23.

[11]FoxSE, AkmatbekovA, HarbertJL, et al., 2020. Pulmonary and cardiac pathology in African American patients with COVID-19: an autopsy series from New Orleans. Lancet Respir Med, 8(7):681-686.

[12]HoffmannM, Kleine-WeberH, SchroederS, et al., 2020. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell, 181(2):271-280.e1-e5.

[13]ImazioM, KlingelK, KindermannI, et al., 2020. COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis? Heart, 106(15):1127-1131.

[14]KonopkaKE, NguyenT, JentzenJM, et al., 2020. Diffuse alveolar damage (DAD) resulting from coronavirus disease 2019 infection is morphologically indistinguishable from other causes of DAD. Histopathology, 77(4):570-578.

[15]LiF, 2016. Structure, function, and evolution of coronavirus spike proteins. Annu Rev Virol, 3(1):237-261.

[16]LiJZ, GongXB, WangZG, et al., 2020. Clinical features of familial clustering in patients infected with 2019 novel coronavirus in Wuhan, China. Virus Res, 286:198043.

[17]LiXW, GengMM, PengYZ, et al., 2020. Molecular immune pathogenesis and diagnosis of COVID-19. J Pharm Anal, 10(2):102-108.

[18]MalikYA, 2020. Properties of coronavirus and SARS-CoV-2. Malays J Pathol, 42(1):3-11.

[19]MeftahiGH, JangraviZ, SahraeiH, et al., 2020. The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging". Inflamm Res, 69(9):825-839.

[20]MenacheryVD, SchaferA, Burnum-JohnsonKE, et al., 2018. MERS-CoV and H5N1 influenza virus antagonize antigen presentation by altering the epigenetic landscape. Proc Natl Acad Sci USA, 115(5):E1012-E1021.

[21]MenterT, HaslbauerJD, NienholdR, 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(2):198-209.

[22]NaqviAAT, FatimaK, MohammadT, et al., 2020. Insights into SARS-CoV-2 genome, structure, evolution, pathogenesis and therapies: structural genomics approach. Biochim Biophys Acta Mol Basis Dis, 1866(10):165878.

[23]OffringaA, MontijnR, SinghS, et al., 2020. The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin-angiotensin system. Eur Heart J Cardiovasc Pharmacother, 6(5):317-325.

[24]OudshoornD, RijsK, RWALLimpens, et al., 2017. Expression and cleavage of middle east respiratory syndrome coronavirus nsp3-4 polyprotein induce the formation of double-membrane vesicles that mimic those associated with coronaviral RNA replication. mBio, 8(6):e01658.

[25]ParkMD, 2020. Immune evasion via SARS-CoV-2 ORF8 protein? Nat Rev Immunol, 20(7):408.

[26]PessoaMSL, LimaCFC, PimentelACF, et al., 2020. Multisystemic infarctions in COVID-19: focus on the spleen. Eur J Case Rep Intern Med, 7(7):001747.

[27]PolakSB, van GoolIC, CohenD, et al., 2020. A systematic review of pathological findings in COVID-19: a pathophysiological timeline and possible mechanisms of disease progression. Mod Pathol, 33(11):2128-2138.

[28]ReichardRR, KashaniKB, BoireNA, et al., 2020. Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)‍-like pathology. Acta Neuropathol, 140(1):1-6.

[29]SekulicM, HarperH, NezamiBG, et al., 2020. Molecular detection of SARS-CoV-2 infection in FFPE samples and histopathologic findings in fatal SARS-CoV-2 cases. Am J Clin Pathol, 154(2):190-200.

[30]ShiY, WangG, CaiXP, et al., 2020. An overview of COVID-19. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 21(5):343-360.

[31]SnijderEJ, van der MeerY, Zevenhoven-DobbeJ, et al., 2006. Ultrastructure and origin of membrane vesicles associated with the severe acute respiratory syndrome coronavirus replication complex. J Virol, 80(12):5927-5940.

[32]SongPP, LiW, XieJQ, et al., 2020. Cytokine storm induced by SARS-CoV-2. Clin Chim Acta, 509:280-287.

[33]SuH, YangM, WanC, et al., 2020. Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney Int, 98(1):219-227.

[34]SuessC, HausmannR, 2020. Gross and histopathological pulmonary findings in a COVID-19 associated death during self-isolation. Int J Legal Med, 134(4):1285-1290.

[35]TanY, TangFQ, 2021. SARS-CoV-2-mediated immune system activation and potential application in immunotherapy. Med Res Rev, 41(2):1167-1194.

[36]TangT, BidonM, JaimesJA, et al., 2020. Coronavirus membrane fusion mechanism offers a potential target for antiviral development. Antiviral Res, 178:104792.

[37]TianSF, XiongY, LiuH, et al., 2020. Pathological study of the 2019 novel coronavirus disease (COVID-19) through postmortem core biopsies. Mod Pathol, 33(6):1007-1014.

[38]VargaZ, FlammerAJ, SteigerP, et al., 2020. Endothelial cell infection and endotheliitis in COVID-19. Lancet, 395(10234):1417-1418.

[39]WuF, ZhaoS, YuB, et al., 2020. A new coronavirus associated with human respiratory disease in China. Nature, 579(7798):265-269.

[40]WuYS, XuXL, ChenZJ, et al., 2020. Nervous system involvement after infection with COVID-19 and other coronaviruses. Brain Behav Immun, 87:18-22.

[41]XuZ, ShiL, WangYJ, et al., 2020. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med, 8(4):420-422.

[42]YangM, ChenS, HuangB, et al., 2020. Pathological findings in the testes of COVID-19 patients: clinical implications. Eur Urol Focus, 6(5):1124-1129.

[43]ZhengY, SunLJ, XuM, et al., 2020. Clinical characteristics of 34 COVID-19 patients admitted to intensive care unit in Hangzhou, China. J Zhejiang Univ-Sci B (Biomed & Biotechnol), 21(5):378-387.

[44]ZhouPC, LiuZG, ChenYH, et al., 2020. Bacterial and fungal infections in COVID-19 patients: a matter of concern. Infect Control Hosp Epidemiol, 41(9):1124-1125.

Open peer comments: Debate/Discuss/Question/Opinion

<1>

Please provide your name, email address and a comment





Journal of Zhejiang University-SCIENCE, 38 Zheda Road, Hangzhou 310027, China
Tel: +86-571-87952783; E-mail: cjzhang@zju.edu.cn
Copyright © 2000 - 2024 Journal of Zhejiang University-SCIENCE