Clinical value of immune-inflammatory parameters to assess the severity of coronavirus disease 2019

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Highlights

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Clinical characteristics and immune-inflammatory parameters were compared between non-severe and severe patients with coronavirus disease 2019 (COVID-19).
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High level of interleukin-6 (IL-6), C-reactive protein (CRP) and hypertension were independent predictors for the severity of COVID-19.
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IL-6 has the highest predictive value among other single immune-inflammatory parameters. The risk model based on IL-6, CRP and hypertension enlarged the predictability.
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The dynamic change of IL-6 in the severe cases were parallel to the amelioration of this disease, implied a potential value for monitoring the process of severe cases.

Abstract

Objective

To explore the clinical value of immune-inflammatory markers to assess the severity of coronavirus disease 2019 (COVID-19).

Methods

127 consecutive hospitalized patients with confirmed COVID-19 were enrolled in this study, and classified into non-severe and severe groups. Demographics, symptoms, underlying diseases and laboratory data were collected and assessed for predictive value.

Results

Of 127 COVID-19 patients, 16 cases (12.60%) were classified into the severe group. High level of interleukin-6 (IL-6), C-reaction protein (CRP) and hypertension were independent risk factors for the severity of COVID-19. The risk model based on IL-6, CRP and hypertension had the highest area under the receiver operator characteristic curve (AUROC). Additionally, the baseline IL-6 was positively correlated with other immune-inflammatory parameters and the dynamic change of IL-6 in the severe cases were parallel to the amelioration of the disease.

Conclusion

Our study showed that high level of IL-6, CRP and hypertension were independent risk factors for assessing the severity of COVID-19. The risk model established upon IL-6, CRP and hypertension had the highest predictability in this study. Besides, IL-6 played a pivotal role in the severity of COVID-19 and had a potential value for monitoring the process of severe cases.

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Most cited references 13

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Origin and evolution of pathogenic coronaviruses

Jie Cui, Fang Li, Zheng-Li Shi (2018)

Severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) are two highly transmissible and pathogenic viruses that emerged in humans at the beginning of the 21st century. Both viruses likely originated in bats, and genetically diverse coronaviruses that are related to SARS-CoV and MERS-CoV were discovered in bats worldwide. In this Review, we summarize the current knowledge on the origin and evolution of these two pathogenic coronaviruses and discuss their receptor usage; we also highlight the diversity and potential of spillover of bat-borne coronaviruses, as evidenced by the recent spillover of swine acute diarrhoea syndrome coronavirus (SADS-CoV) to pigs.

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A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury

Keiji Kuba, Yumiko Imai, Shuan Rao … (2005)

During several months of 2003, a newly identified illness termed severe acute respiratory syndrome (SARS) spread rapidly through the world 1,2,3 . A new coronavirus (SARS-CoV) was identified as the SARS pathogen 4,5,6,7 , which triggered severe pneumonia and acute, often lethal, lung failure 8 . Moreover, among infected individuals influenza such as the Spanish flu 9,10 and the emergence of new respiratory disease viruses 11,12 have caused high lethality resulting from acute lung failure 13 . In cell lines, angiotensin-converting enzyme 2 (ACE2) has been identified as a potential SARS-CoV receptor 14 . The high lethality of SARS-CoV infections, its enormous economic and social impact, fears of renewed outbreaks as well as the potential misuse of such viruses as biologic weapons make it paramount to understand the pathogenesis of SARS-CoV. Here we provide the first genetic proof that ACE2 is a crucial SARS-CoV receptor in vivo. SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway. These results provide a molecular explanation why SARS-CoV infections cause severe and often lethal lung failure and suggest a rational therapy for SARS and possibly other respiratory disease viruses. Supplementary information The online version of this article (doi:10.1038/nm1267) contains supplementary material, which is available to authorized users.

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Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology

Rudragouda Channappanavar, Stanley Perlman (2017)

Human coronaviruses (hCoVs) can be divided into low pathogenic and highly pathogenic coronaviruses. The low pathogenic CoVs infect the upper respiratory tract and cause mild, cold-like respiratory illness. In contrast, highly pathogenic hCoVs such as severe acute respiratory syndrome CoV (SARS-CoV) and Middle East respiratory syndrome CoV (MERS-CoV) predominantly infect lower airways and cause fatal pneumonia. Severe pneumonia caused by pathogenic hCoVs is often associated with rapid virus replication, massive inflammatory cell infiltration and elevated pro-inflammatory cytokine/chemokine responses resulting in acute lung injury (ALI), and acute respiratory distress syndrome (ARDS). Recent studies in experimentally infected animal strongly suggest a crucial role for virus-induced immunopathological events in causing fatal pneumonia after hCoV infections. Here we review the current understanding of how a dysregulated immune response may cause lung immunopathology leading to deleterious clinical manifestations after pathogenic hCoV infections.

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Author and article information

Contributors

Zhe Zhu

Ting Cai

Lingyan Fan

Kehong Lou

Xin Hua

Zuoan Huang

Guosheng Gao

Journal

Journal ID (nlm-ta): Int J Infect Dis

Journal ID (iso-abbrev): Int. J. Infect. Dis

Title: International Journal of Infectious Diseases

Publisher: The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.

ISSN (Print): 1201-9712

ISSN (Electronic): 1878-3511

Publication date PMC-release: 22 April 2020

Publication date (Electronic): 22 April 2020

Affiliations

[a ]Department of Blood Transfusion, HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, PR China

[b ]Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo, PR China

[c ]Key Laboratory of Diagnosis and Treatment of Digestive System Tumors of Zhejiang Province, Ningbo, PR China

[d ]Department of Acute Infectious Diseases. HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, PR China

[e ]Department of Clinical Laboratory, HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, PR China

[f ]Department of Experimental Medical Science, HwaMei Hospital, University of Chinese Academy of Sciences, Ningbo, PR China

Author notes

[* ]Corresponding author. Department of Clinical Laboratory, HwaMei Hospital, University of Chinese Academy of Sciences, 41 Xibei street, Ningbo, PR China. 495926922@ 123456qq.com

[1]

Contributed equally.

Article

Publisher ID: S1201-9712(20)30257-5

DOI: 10.1016/j.ijid.2020.04.041

PMC ID: 7195003

PubMed ID: 32334118

SO-VID: 8b5237f2-46c5-4e9c-ba75-02fe5f6717e7

License:

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

History

Date received : 1 April 2020

Date revision received : 15 April 2020

Date accepted : 17 April 2020

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Clinical value of immune-inflammatory parameters to assess the severity of coronavirus disease 2019

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Highlights

Abstract

Objective

Methods

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Conclusion

Related collections

Novel Coronavirus Disease COVID-19

Most cited references 13

Origin and evolution of pathogenic coronaviruses

A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury

Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology

Author and article information

Contributors

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Article

History

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Cited by 204