About: Clinical Characteristics and Immune Injury Mechanisms in 71 Patients with COVID-19

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About: Clinical Characteristics and Immune Injury Mechanisms in 71 Patients with COVID-19 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Clinical Characteristics and Immune Injury Mechanisms in 71 Patients with COVID-19
Creator	Wu, Yingjie Zhou, Fuling Huang, Xiaoxing Qin, Hong Shao, Liang Sun, Jiaxing Lei, Yufei Li, Xinran Muhammad, Jamal Xie, Tian Zeng, Xingruo Zhang, Qiuping Lei, Xie Li, Muhammad Wu, Citation
Source	Medline; PMC
abstract	The outbreak of coronavirus disease 2019 (COVID-19), caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a threat to global health. The mortality rate of severely ill patients in the early stage is 32.5%. The exacerbation of the condition and death of patients are closely associated with inflammatory cytokine storms, which are caused by excessive activation of the immune and complement systems as well as the coinfection of other pathogens. However, the immunological characteristics and the mechanisms underlying inflammatory storms have not been well elucidated. Here, we analyzed the clinical and immunological characteristics of 71 confirmed COVID-19 patients. Based on the National Health Commission of China (NHCC) guidelines, patients were stratified into mild and severe types. We compared the clinical and laboratory data obtained from electronic medical records between the two types. In regard to the hematological parameters, COVID-19 patients showed decreased erythrocyte count, hemoglobin, hematocrit, lymphocyte count, eosinophil count, and complement C1q, whereas neutrophils, C-reactive protein, and procalcitonin were significantly increased, especially in severe cases. We also found that CD3(+) CD4(+) T lymphocytes, CD3(+) CD8(+) T lymphocytes, CD19(+) B lymphocytes, and CD16(+) CD56(+) NK cells in the peripheral blood of all patients were decreased. In addition, CD3(+) CD8(+) T lymphocytes, CD16(+) CD56(+) NK cells, and complement C1q in severely ill patients decreased more significantly. Additionally, interleukin 6 (IL-6) elevation was particularly prominent in all patients, especially in severe cases. These results suggest that CD3(+) CD8(+) T lymphocytes, CD16(+) CD56(+) NK cells, C1q as well as IL-6 may play critical roles in the inflammatory cytokine storm. The dysregulation of these aforementioned immune parameters, along with bacterial coinfection, were the important causes of exacerbation of the patients’ condition and death. This study improves our understanding of the immune dysregulation of COVID-19 and provides potential immunotherapeutic strategies. IMPORTANCE The dysregulation of CD3(+) CD8(+) T lymphocytes, CD16(+) CD56(+) NK cells, C1q as well as IL-6, along with bacterial coinfection, were important causes of exacerbation of the patients’ condition and death.
has issue date	2020-07-15(xsd:dateTime)
bibo:doi	10.1128/msphere.00362-20
bibo:pmid	32669467
has license	cc-by
sha1sum (hex)	4c7eadb064da075d04739ef54c65358848825f1b
schema:url	https://doi.org/10.1128/msphere.00362-20
resource representing a document's title	Clinical Characteristics and Immune Injury Mechanisms in 71 Patients with COVID-19
has PubMed Central identifier	PMC7364211
has PubMed identifier	32669467
schema:publication	mSphere
resource representing a document's body	covid:4c7eadb064da075d04739ef54c65358848825f1b#body_text
is schema:about of	named entity 'caused' named entity 'immune' named entity 'ill' named entity 'COVID-19' named entity 'cases' named entity 'roles' named entity 'severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)' named entity 'stratified' named entity 'Mechanisms' named entity 'INFLAMMATORY CYTOKINE' named entity 'UNDERSTANDING' named entity 'INFLAMMATORY' named entity 'TYPES' named entity 'THESE' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2' named entity 'ASSOCIATED WITH' named entity 'IL-6' named entity 'LABORATORY DATA' named entity 'THREAT' named entity 'CD19' named entity 'SEVERE' named entity 'EARLY STAGE' named entity 'ACTIVATION' named entity 'BASED' named entity 'NOVEL CORONAVIRUS' named entity 'T lymphocytes' named entity 'coronavirus disease 2019' named entity 'patients' named entity 'procalcitonin' named entity 'T lymphocytes' named entity 'count' named entity 'erythrocyte count' named entity 'CD16' named entity 'lymphocyte count' named entity 'ill' named entity 'CD56' named entity 'CD16' named entity 'lymphocytes' named entity 'coronavirus disease 2019' named entity 'coronavirus' named entity 'CD56' named entity 'coinfection' named entity 'NK cells' named entity 'C1q' named entity 'severe acute respiratory syndrome coronavirus 2' named entity 'CD19' named entity 'procalcitonin' named entity 'lymphocytes' named entity 'immune dysregulation' named entity 'electronic medical records' named entity 'CD16' named entity 'IL-6' named entity 'Clinical Characteristics' named entity 'CD8' named entity 'flow cytometer' named entity 'pneumonia' named entity 'Hangzhou' named entity 'white blood cell (WBC) count' named entity 'eosinophil' named entity 'Lymphocyte' named entity 'expression levels' named entity 'IL-6' named entity 'CD16' named entity 'lymphocyte' named entity 'MERS' named entity 'CD3' named entity 'fatality rate'

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