Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China
Open accessAbstract
Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0-58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0-13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.
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Myocardial damage similar to myocarditis was one of the first complications reported from patients with COVID-19 in Wuhan, China, at the beginning of the pandemic.
“Myocardial damage similar to myocarditis was one of the first complications reported from patients with COVID19 in Wuhan, China, at the beginning of the pandemic.”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [66]
The Results report acute cardiac injury as a complication in five of 41 patients in the early Wuhan cohort. The Methods define cardiac injury by elevated biomarkers or new ECG or echocardiographic abnormalities; the paper does not characterize it as myocarditis-like. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe most common clinical presentation of severe COVID-19 is viral pneumonia featuring fever, cough, dyspnoea, hypoxemia, and bilateral infiltrates on chest radiographs.
“Evidence shows that the most common clinical presentation of severe COVID-19 is viral pneumonia featuring fever, cough, dyspnoea, hypoxemia, and bilateral infiltrates on chest radiographs [2–4].”
From Effects of short-term breathing exercises on respiratory recovery in patients with COVID-19: a quasi-experimental study (2022) · cites this paper as [2]
The Results report pneumonia in all 41 patients, frequent fever and cough, dyspnoea in 12 of 13 ICU patients, and bilateral chest-radiograph involvement in all 13. The paper reports refractory hypoxaemia in only two patients and describes a small hospitalised cohort; it does not establish that the full combination is the most common presentation of severe COVID-19 generally. (LLM, conf=0.84)
Experimental — accuracy not yet measuredCoronavirus disease 2019 (COVID-19) is a highly infectious respiratory tract disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
“Coronavirus disease 2019 (COVID-19) is a highly infectious respiratory tract disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1, 2].”
From Effects of short-term breathing exercises on respiratory recovery in patients with COVID-19: a quasi-experimental study (2022) · cites this paper as [2]
The Introduction identifies 2019-nCoV in lower respiratory tract samples from patients with pneumonia, supporting the claim that a novel coronavirus caused respiratory disease. The Discussion says evidence indicated human transmission but describes efficient human transmission as a concern, not an established finding; it does not support calling the disease “highly infectious.” The paper uses the earlier name 2019-nCoV rather than SARS-CoV-2. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCOVID-19 patients rapidly deteriorate to acute respiratory failure.
“This is because the respiratory problems experienced by patients with COVID-19 significantly differ from other respiratory conditions (e.g., dry cough is common [4, 19]) and COVID-19 patients' rapid deterioration to acute respiratory failure [2–4].”
From Effects of short-term breathing exercises on respiratory recovery in patients with COVID-19: a quasi-experimental study (2022) · cites this paper as [2]
The Discussion reports that patients with severe illness developed acute respiratory distress syndrome (ARDS), in some cases as soon as two days after admission. The Results show ARDS in 12 of 41 patients (29%). This supports rapid deterioration in a subset of the hospitalized cohort, but not the unqualified implication that COVID-19 patients generally deteriorate to acute respiratory failure. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSevere respiratory symptoms can cause respiratory failure (ARDS), which can lead to death unless promptly managed using ventilation at ICU.
“As mentioned before, severe respiratory symptoms can cause respiratory failure (ARDS), which can lead to death unless promptly managed using ventilation at ICU [2, 3, 6].”
From Effects of short-term breathing exercises on respiratory recovery in patients with COVID-19: a quasi-experimental study (2022) · cites this paper as [2]
The Discussion reports that severely ill patients developed ARDS and required ICU admission and oxygen therapy; the Results report mechanical ventilation in four patients and six deaths. The paper does not establish that prompt ICU ventilation prevents death or that death follows unless it is provided. (LLM, conf=0.86)
Experimental — accuracy not yet measured
In patients with COVID-19, low blood oxygen levels are associated with rapid deterioration to acute respiratory distress or failure, leading to death unless it is managed immediately [2-4].
“In patients with COVID-19, low blood oxygen levels are associated with rapid deterioration to acute respiratory distress or failure, leading to death unless it is managed immediately [2–4].”
From Effects of short-term breathing exercises on respiratory recovery in patients with COVID-19: a quasi-experimental study (2022) · cites this paper as [2]
The Discussion (page not provided) says severe patients developed ARDS, sometimes within two days of admission, and six of 41 patients died. The Results also report refractory hypoxaemia in two patients who received salvage therapy. The paper does not establish that low oxygen levels predict rapid deterioration or that death follows unless they are managed immediately. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe severity of COVID-19 is associated with an increased level of inflammatory cytokines, such as IL-6, GM-CSF and TNFα.
“Consistent with the notion that severe COVID-19 is a cytokine storm syndrome (12–17, 336), the severity of COVID-19 is associated with an increased level of inflammatory cytokines, such as IL-6, granulocyte macrophage colony-stimulating factor (GM-CSF) and TNFα (333, 337).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [333]
The Discussion reports higher TNFα concentrations in patients requiring ICU care than in those who did not, linking elevated cytokines with disease severity. It names GCSF, not GM-CSF, in that comparison; the Methods list GCSF and GMCSF separately. The paper also does not identify IL-6 as higher in its ICU patients. (LLM, conf=0.90)
Experimental — accuracy not yet measuredOn Jan 11, 2020, a scientist in China posted the genomic sequence of SARS-CoV-2 to a public database, and Chinese authorities posted the sequence the next day.
“On Jan 11, 2020, a scientist in China posted the genomic sequence of SARS-CoV-2 to a public database, and Chinese authorities posted the sequence the next day.76, 77”
From The Lancet Commission on lessons for the future from the COVID-19 pandemic (2022) · cites this paper as [77]
Among patients who developed severe disease, median time to dyspnea was 5 to 8 days, median time to ARDS was 8 to 12 days, and median time to intensive care unit admission was 10 to 12 days after symptom onset.
“Additional studies found that, among patients who developed severe disease, the median time to dyspnea was 5 to 8 days, the median time to ARDS was 8 to 12 days, and the median time to intensive care unit admission was 10 to 12 days after symptom onset (68–70).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [68]
Higher concentrations of these cytokines appear to indicate a more severe clinical course.
“Higher concentrations of these cytokines seem to suggest a more severe clinical course (Huang et al., 2020).”
From Anxiety and depression in COVID-19 survivors: role of inflammatory and clinical predictors (2020) · cites this paper as Huang et al., 2020
Cytokine storm is manifested by increased plasma concentrations of IL-2, IL-7, IL-10, G-CSF, CXCL10, CCL2, CCL3, and TNF-α.
“which is manifested by the increased plasma concentrations of IL-2, IL-7, IL-10, G-CSF, CXCL10, CCL2, CCL3, and TNF-α (Hui and Zumla, 2019; Huang et al., 2020; Li G. et al., 2020).”
From Oral Microbiome and SARS-CoV-2: Beware of Lung Co-infection (2020) · cites this paper as Huang et al., 2020
Like SARS-CoV and MERS-CoV, SARS-CoV-2 can also induce excessive and aberrant non-effective host immune responses that are associated with severe lung pathology, and lead to death.
“Like SARS-CoV and MERS-CoV, SARS-CoV-2 can also induce excessive and aberrant non-effective host immune responses that are associated with severe lung pathology, and lead to death (Hui and Zumla, 2019; Huang et al., 2020).”
From Oral Microbiome and SARS-CoV-2: Beware of Lung Co-infection (2020) · cites this paper as Huang et al., 2020
Patients infected with SARS-CoV-2 present elevated levels of IL-6, IL-10, IL-1β, INF-γ, CCL2, TNF-α, CXCL10, CCL7, IL-1 receptor antagonist and IL-2 receptor, supposedly associated with disease severity.
“Patients infected with SARS-CoV-2 present elevated levels of IL-6, IL-10, IL-1β, INF-γ, CCL2, TNF-α, CXCL10, CCL7, IL-1 receptor antagonist and IL-2 receptor, supposedly associated with disease severity [9, 98–105].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [98]
Viral binding to ACE2 receptors leads to significant changes in fluid-coagulation balance, including increased IL6 levels, cytokine storm, expression of tissue inhibitor of plasminogen-1 and tissue factor, and triggering of the coagulation system through binding to clotting factor VIIa.
“Viral binding to ACE2Receptors leads to significant changes in fluid-coagulation balance: reduction in Ang 2 degradation leads to increased Il6 levels, and the onset of storm cytokines, such as IL-2, IL-7, IL-10, granulocyte colony-stimulating factor, IgG -induced protein 10, monocyte chemoattractant protein-1, macrophage inflammatory protein 1-alpha, and tumor necrosis factor α [67], but also in”
From Acute mesenteric ischemia in COVID-19 patients (2021) · cites this paper as [67]
Serum cytokine levels elevated in patients with Covid-19-associated cytokine storm include interleukin-1β, interleukin-6, IP-10, TNF, interferon-γ, macrophage inflammatory protein 1α and 1β, and VEGF.
“Serum cytokine levels that are elevated in patients with Covid-19–associated cytokine storm include interleukin-1β, interleukin-6, IP-10, TNF, interferon-γ, macrophage inflammatory protein (MIP) 1α and 1β, and VEGF.89,90”
From Cytokine storm (2020) · cites this paper as [89]
Wang et al. provide a detailed description of major signs and symptoms of overt disease but fail to give an account of minor symptoms that may be present at earlier stages of the infection.
“The authors provide a detailed description of major signs and symptoms of overt disease [2, 3], but fail to give an account of minor symptoms that may be present at earlier stages of the infection.”
From Self-reported Olfactory and Taste Disorders in Patients With Severe Acute Respiratory Coronavirus 2 Infection: A Cross-sectional Study (2020) · cites this paper as [2]
Patients having surgery are a vulnerable group at risk of SARS-CoV-2 exposure in hospital and might be particularly susceptible to subsequent pulmonary complications, due to pro-inflammatory cytokine and immunosuppressive responses to surgery and mechanical ventilation.
“Patients having surgery are a vulnerable group at risk of SARS-CoV-2 exposure in hospital and might be particularly susceptible to subsequent pulmonary complications, due to the pro-inflammatory cytokine and immunosuppressive responses to surgery and mechanical ventilation.3, 4”
From Mortality and pulmonary complications in patients undergoing surgery with perioperative SARS-CoV-2 infection: an international cohort study (2020) · cites this paper as [3]
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“ARDS in COVID-19 is considered the result of cytokine storm (12–17), re-sembling the disease caused by SARS-CoV-1 and Middle East respiratory syndrome coronavirus (MERS-CoV) (335).”
BackgroundInfluential
- Authors
- Huang, C., Wang, Y., Li, X., Ren, L., Zhao, J., Hu, Y., Zhang, L., Fan, G., Xu, J., Gu, X., Cheng, Z., Yu, T., Xia, J., Wei, Y., Wu, W., Xie, X., Yin, W., Li, H., Liu, M., Xiao, Y., Gao, H., Guo, L., Xie, J., Wang, G., Jiang, R., Gao, Z., Jin, Q., Wang, J., & Cao, B.
- Affiliations
- Jinyintan Hospital (CN)
- Capital Medical University (CN)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Tongji Hospital (CN)
- Central Hospital of Wuhan (CN)
- Tsinghua University (CN)
- Zhongnan Hospital of Wuhan University (CN)
- China-Japan Friendship Hospital (CN)
- Peking University First Hospital (CN)
- Peking University People's Hospital (CN)
- Corresponding author
- Wang, Jianwei
- ORCID
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2020-02
- Volume
- 395
- Issue
- 10223
- Pages
- 497-506
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC7159299
- OpenAlex
- W3001118548
- Cited by
- 48,884
- References
- 25
- Citations by year
- 2026: 679 · 2025: 1388 · 2024: 2819 · 2023: 5030 · 2022: 8174 · 2021: 13463 · 2020: 17217 · 2019: 36 · 2018: 8 · 2017: 3 · 2016: 1 · 2015: 5 · 2014: 1 · 2013: 4 · 2012: 5
- FWCI
- 1395.14
- Type
- journal article
- Language
- en
- Update notices
- erratum (2020-02-15)
- Open access
- bronze
- doi.org
- Locations
- The Lancet (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zenodo (CERN European Organization for Nuclear Research)
- Funders
- Chinese Academy of Medical Sciences (2016‐I2M‐1‐014, CIFMS 2018-I2M-1-003, 2018-I2M-1-003)
- National Health Commission of the People's Republic of China
- National Key Research and Development Program of China (2020YFC0841300, 2018YFC1200102)
- Topics
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Keywords
- SARS-CoV-2, COVID-19 pandemic, clinical features, pneumonia, lymphopenia, acute respiratory distress syndrome, intensive care unit admission, mortality, risk factors, comorbidities, Huanan Seafood Market, family clusters, Wuhan, chest CT findings, treatment outcomes, clinical outcomes, laboratory-confirmed infections
- MeSH terms
- COVID-19, Adult, Aged, China, Cough, Female, Fever, Hospitalization, Humans, Intensive Care Units, Male, Middle Aged, Pneumonia, Viral, Prognosis, Respiratory Distress Syndrome, Radiography, Thoracic, Time Factors, Tomography, X-Ray Computed, Comorbidity, Age Distribution, Coronavirus Infections, Young Adult, Myalgia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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