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1.
Signal Transduct Target Ther ; 7(1): 83, 2022 03 11.
Article in English | MEDLINE | ID: covidwho-1740428

ABSTRACT

SARS-CoV-2 induced marked lymphopenia in severe patients with COVID-19. However, whether lymphocytes are targets of viral infection is yet to be determined, although SARS-CoV-2 RNA or antigen has been identified in T cells from patients. Here, we confirmed that SARS-CoV-2 viral antigen could be detected in patient peripheral blood cells (PBCs) or postmortem lung T cells, and the infectious virus could also be detected from viral antigen-positive PBCs. We next prove that SARS-CoV-2 infects T lymphocytes, preferably activated CD4 + T cells in vitro. Upon infection, viral RNA, subgenomic RNA, viral protein or viral particle can be detected in the T cells. Furthermore, we show that the infection is spike-ACE2/TMPRSS2-independent through using ACE2 knockdown or receptor blocking experiments. Next, we demonstrate that viral antigen-positive T cells from patient undergone pronounced apoptosis. In vitro infection of T cells induced cell death that is likely in mitochondria ROS-HIF-1a-dependent pathways. Finally, we demonstrated that LFA-1, the protein exclusively expresses in multiple leukocytes, is more likely the entry molecule that mediated SARS-CoV-2 infection in T cells, compared to a list of other known receptors. Collectively, this work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID-19 patients.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/metabolism , SARS-CoV-2/metabolism , T-Lymphocytes/metabolism , Animals , Caco-2 Cells , Chlorocebus aethiops , Humans , Vero Cells
2.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-312646

ABSTRACT

Objective: To investigate the value of changes of pulmonary circulation in CT imaging in evaluating the severity and tendency of 2019 novel coronavirus disease (COVID-19) pneumonia. Methods: : This retrospective study analyzed 99 severe and critical COVID-19 pneumonia patients including the 47 improved cases and 52 dead cases. Demographic data, laboratory findings, comorbidities, and CT imaging features including the diameters of pulmonary vein (PV), pulmonary artery (PA) and ascending aorta were collected and assessed. Results: : The PV diameters of the deceased patients were larger than recovered patients in the severe phase. Compared with the severe phase in the improvement group, the diameters of the pulmonary veins during the improved phase were smaller, and the total CT scores were significantly decreased (p < 0.001). Instead, there was no significant difference in the ratio of main PA to aorta diameter between the recovered group and the deceased group, nor did the self control of the recovered group and the deceased group ( p > 0.05). Construction of a ROC curve yielded an optimal cut-off value of the PV diameters for prediction of survival ( p < 0.05). Conclusion: The changes of the PV diameters might indirectly reflect the activity of pulmonary inflammation and cardiac insufficiency. Pulmonary manifestations of severe and critical COVID-19 pneumonia might be related to myocardial injury and cardiac insufficiency, expecially accompanied by dilated PVs. Evaluation of changes in pulmonary circulation by chest CT images may be considered as a useful tool for determining the severity, fatal outcome and tendency of COVID-19. Key words: COVID-19, pneumonia, pulmonary circulation, Computed Tomography

3.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-325094

ABSTRACT

Background: Coronavirus Disease-2019 (COVID-19) has caused considerable morbidity and mortality. Hence, there is an urgency to find effective treatment. Tocilizumab, an inhibitor of IL-6, has been widely proposed as a treatment of severely ill patients without robust evidence supporting its use. Methods: In this multicentre, retrospective, cohort study, we included 5,235 adult patients who were admitted to 3 hospitals in Wuhan, China with confirmed COVID-19 from January 20 to March 18, 2020 . 65 patients in tocilizumab group and 130 patients in non-tocilizumab group were propensity score matched at a ratio of 2:1 based on age, sex, and comorbidities. Detailed demographic data, comorbidities, radiological and laboratory parameters, complications and treatments were compared between tocilizumab group and non-tocilizumab group. Furthermore, univariable and multivariable Logistic and Cox regression models were used to explore the risk of complications and in-hospital death associated with tocilizumab. Findings: During the follow-up, patients in non-tocilizumab group were more likely to develop into death (42 [32·31%] vs 14 [21·54%]). After adjusting for confounding, the detected risk for in-hospital death was lower in the tocilizumab group versus the non-tocilizumab group (HR=0·47;95% CI=0·25-0·90;p=0·023). In the multivariable logistic regression model, use of tocilizumab was associated with a lower risk of ARDS (OR=0 · 23;95% CI=0·11-0·45;p<0·0001). Before treatment the patients had heightened inflammation and more dysregulated immune cells, which might aggravate disease progression. However, abnormally elevated IL-6, CRP, fibrinogen and APTT decreased in COVID-19 patients after treatment. And the counts of lymphocytes and immune cells subset in peripheral blood, which decreased in patients, returned to normal after treatment. No obvious complications were observed. Interpretation: Tocilizumab may be of value in improving outcomes in severe patients of COVID-19, which provided a novel strategy for COVID-19-induced cytokine release syndrome (CRS). Our preliminary data could inform bedside decisions until more data from randomized, controlled clinical trials becomes available.Funding Statement: SARS-CoV-2 Pneumonia Emergency Technology Public Relations Project of Tongji Medical College, Huazhong University of Science and Technology (No. 2020kfyXGYJ043) and National Key Research and Development Plan for the Emergency Management of Novel Coronavi rus Pneumonia, China (No. 2020YFC0845100).Declaration of Interests: The authors report no conflicts of interest.Ethics Approval Statement: This study was approved by the Ethics Committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (TJ-C20200108) and granted a waiver of informed consent from study participants.

4.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-324976

ABSTRACT

Objectives: To investigate the chest high-resolution CT (HRCT) findings in coronavirus disease 2019 (COVID-19) pneumonia patients with acute respiratory distress syndrome (ARDS) and to evaluate its relationship with clinical outcome. Materials: and Methods In this retrospective study, seventy-nine COVID-19 patients with ARDS were recruited. Clinical data were extracted from electronic medical records and analyzed. HRCT scans, obtained within 3 days before clinical ARDS onset, were evaluated by three independent observers and graded into six findings according to the extent of fibroproliferation. Multivariable Cox proportional hazard regression analysis was used to assess the independent predictive value of the CT score and radiologically fibroproliferation. Patient survival was determined by Kaplan-Meier analysis. Results: : Compared with survivors, non-survivors showed higher of lung fibroproliferation, whereas there no significant differences in the area of increased attenuation without traction bronchiolectasis or bronchiectasis. A HRCT score <230 enabled prediction of survival with 73.5% sensitivity and 93.3% specificity (AUC= 0.9;95% CI 0.831 to 0.968). Multivariate Cox proportional hazards model showed that the HRCT score is a significant independent risk factor for mortality (HR 13.007;95% CI 3.935 to 43.001). Kaplan-Meier analysis revealed HRCT score≥230 was associated with higher fatality rate. Organ injury occurred less frequently in patients with HRCT score<230 compared to those with HRCT score≥230. Conclusion: Early pulmonary fibroproliferative changes in HRCT predicts increased mortality and susceptibility to organ injury in COVID-19 pneumonia patients with early ARDS.

6.
J Glob Health ; 11: 05006, 2021 Mar 27.
Article in English | MEDLINE | ID: covidwho-1173056

ABSTRACT

BACKGROUND: In December 2019, coronavirus disease 2019 (COVID-19) emerged in Wuhan city and rapidly spread throughout China. So far, it has caused ~ 4000 deaths in this country. We aimed to systematically characterize clinical features and determine risk factors of sudden death for COVID-19 patients. METHODS: Deceased patients with COVID-19 in Tongji hospital from January 22 to March 23, 2020 were extracted. Patients who died within 24 hours after admission were identified as sudden deaths, and the others formed non-sudden deaths. The differences in clinical characteristics between the two groups were estimated. Risk factors associated with sudden deaths were explored by logistic regression. RESULTS: 281 deceased patients were enrolled in this study. Sudden death occurred in 28 (10.0%) patients, including 4 (14.3%) admitted to the intensive care unit. Fatigue was more common in sudden deaths (11, 47.8%) than in non-sudden deaths (40, 17.2%). Both the count and percentage of eosinophils were lower in sudden deaths than that in non-sudden deaths (P = 0.006 and P = 0.004). Compared with non-sudden deaths, sudden deaths had higher plasma levels of procalcitonin, C-reactive protein, D-dimer, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, lactate dehydrogenase, alkaline phosphatase and N-terminal pro-brain natriuretic peptide. There were not significant differences in gender, age, chest CT image features and comorbidities observed. CONCLUSIONS: The differences between the two groups suggested more severe systemic inflammation, multi-organ dysfunction, especially impaired liver and heart function in COVID-19 patients who died suddenly after admission. More researches are needed to verify these points.


Subject(s)
COVID-19/mortality , Death, Sudden/epidemiology , Patient Admission/statistics & numerical data , SARS-CoV-2 , Aged , Cause of Death , China/epidemiology , Death, Sudden/etiology , Female , Hospital Mortality , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors
7.
Ther Adv Chronic Dis ; 12: 2040622320982171, 2021.
Article in English | MEDLINE | ID: covidwho-1093950

ABSTRACT

OBJECTIVES: To investigate the chest high-resolution computed tomography (HRCT) findings in coronavirus disease 2019 (COVID-19) pneumonia patients with acute respiratory distress syndrome (ARDS) and to evaluate its relationship with clinical outcome. MATERIALS AND METHODS: In this retrospective study, 79 COVID-19 patients with ARDS were recruited. Clinical data were extracted from electronic medical records and analyzed. HRCT scans, obtained within 3 days before clinical ARDS onset, were evaluated by three independent observers and graded into six findings according to the extent of fibroproliferation. Multivariable Cox proportional hazard regression analysis was used to assess the independent predictive value of the computed tomography (CT) score and radiological fibroproliferation. Patient survival was determined by Kaplan-Meier analysis. RESULTS: Compared with survivors, non-survivors showed higher rates of lung fibroproliferation, whereas there were no significant differences in the area of increased attenuation without traction bronchiolectasis or bronchiectasis. A HRCT score <230 enabled the prediction of survival with 73.5% sensitivity and 93.3% specificity, 100% negative predictive value (NPP), 83.3% positive predictive value (PPV) and 88.6% accuracy (Area Under the Curve [AUC] = 0.9; 95% confidence Interval [CI] 0.831-0.968). A multivariate Cox proportional hazards model showed that the HRCT score is a significant independent risk factor for mortality (Hazard Ratio [HR] 9.94; 95% CI 4.10-24.12). Kaplan-Meier analysis revealed that a HRCT score ⩾230 was associated with a higher fatality rate. Organ injury occurred less frequently in patients with a HRCT score <230 compared to those with a HRCT score ⩾230. CONCLUSION: Early pulmonary fibroproliferative signs on HRCT are associated with increased mortality and susceptibility to organ injury in COVID-19 pneumonia patients with early ARDS.

8.
Sci Adv ; 7(1)2021 01.
Article in English | MEDLINE | ID: covidwho-1066781

ABSTRACT

Despite past extensive studies, the mechanisms underlying pulmonary fibrosis (PF) still remain poorly understood. Here, we demonstrated that lungs originating from different types of patients with PF, including coronavirus disease 2019, systemic sclerosis-associated interstitial lung disease, and idiopathic PF, and from mice following bleomycin (BLM)-induced PF are characterized by the altered methyl-CpG-binding domain 2 (MBD2) expression in macrophages. Depletion of Mbd2 in macrophages protected mice against BLM-induced PF. Mbd2 deficiency significantly attenuated transforming growth factor-ß1 (TGF-ß1) production and reduced M2 macrophage accumulation in the lung following BLM induction. Mechanistically, Mbd2 selectively bound to the Ship promoter in macrophages, by which it repressed Ship expression and enhanced PI3K/Akt signaling to promote the macrophage M2 program. Therefore, intratracheal administration of liposomes loaded with Mbd2 siRNA protected mice from BLM-induced lung injuries and fibrosis. Together, our data support the possibility that MBD2 could be a viable target against PF in clinical settings.


Subject(s)
COVID-19/metabolism , DNA-Binding Proteins/metabolism , Macrophages/metabolism , Pulmonary Fibrosis/metabolism , Animals , Bleomycin/pharmacology , Carcinoma, Non-Small-Cell Lung/metabolism , Fibrosis , Gene Expression Profiling , Gene Expression Regulation , Humans , Liposomes/chemistry , Lung Diseases, Interstitial/metabolism , Lung Neoplasms/metabolism , Macrophages/virology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Pulmonary Fibrosis/virology , RNA, Small Interfering/metabolism , Scleroderma, Systemic/metabolism , Signal Transduction , Transforming Growth Factor beta1/metabolism
10.
J Med Virol ; 92(11): 2742-2750, 2020 11.
Article in English | MEDLINE | ID: covidwho-967135

ABSTRACT

Since the outbreak of 2019 novel coronavirus (SARS-CoV-2) pneumonia, many patients with underlying disease, such as interstitial lung disease (ILD), were admitted to Tongji hospital in Wuhan, China. To date, no data have ever been reported to reflect the clinical features of Corona Virus Disease 2019 (COVID-19) among these patients with preexisting ILD. We analyzed the incidence and severity of COVID-19 patients with ILD among 3201 COVID-19 inpatients, and compared two independent cohorts of COVID-19 patients with pre-existing ILD (n = 28) and non-ILD COVID-19 patients (n = 130). Among those 3201 COVID-19 inpatients, 28 of whom were COVID-19 with ILD (0.88%). Fever was the predominant symptom both in COVID-19 with ILD (81.54%) and non-ILD COVID-19 patients (72.22%). However, COVID-19 patients with ILD were more likely to have cough, sputum, fatigue, dyspnea, and diarrhea. A very significantly higher number of neutrophils, monocytes, interleukin (IL)-8, IL-10, IL-1ß, and D-Dimer was characterized in COVID-19 with ILD as compared to those of non-ILD COVID-19 patients. Furthermore, logistic regression models showed neutrophils counts, proinflammatory cytokines (tumor necrosis factor-alpha, IL6, IL1ß, IL2R), and coagulation dysfunction biomarkers (D-Dimer, PT, Fbg) were significantly associated with the poor clinical outcomes of COVID-19. ILD patients could be less vulnerable to SARS-CoV-2. However, ILD patients tend to severity condition after being infected with SARS-CoV-2. The prognosis of COVID-19 patients with per-existing ILD is significantly worse than that of non-ILD patients. And more, aggravated inflammatory responses and coagulation dysfunction appear to be the critical mechanisms in the COVID-19 patients with ILD.


Subject(s)
COVID-19/epidemiology , Lung Diseases, Interstitial/virology , Adult , COVID-19/physiopathology , China , Cough/epidemiology , Diarrhea/epidemiology , Female , Fever/epidemiology , Humans , Inflammation/complications , Inflammation/immunology , Logistic Models , Lung Diseases, Interstitial/epidemiology , Male , Prognosis , Retrospective Studies , Severity of Illness Index
11.
J Immunol ; 206(3): 599-606, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-969665

ABSTRACT

The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable morbidity and mortality. Tocilizumab, an inhibitor of IL-6, has been widely repurposed as a treatment of severely ill patients without robust evidence supporting its use. In this study, we aimed to systematically describe the effectiveness of treatment and prevention of the cytokine storms in COVID-19 patients with tocilizumab. In this multicentered retrospective and observational cohort study, 65 patients with COVID-19 receiving tocilizumab and 130 not receiving tocilizumab were propensity score matched at a ratio of 2:1 based on age, sex, and comorbidities from January 20, 2020 to March 18, 2020 in Wuhan, China. After adjusting for confounding, the detected risk for in-hospital death was lower in the tocilizumab group versus nontocilizumab group (hazard ratio = 0.47; 95% confidence interval = 0.25-0.90; p = 0.023). Moreover, use of tocilizumab was associated with a lower risk of acute respiratory distress syndrome (odds ratio = 0.23; 95% confidence interval = 0.11-0.45; p < 0.0001). Furthermore, patients had heightened inflammation and more dysregulated immune cells before treatment, which might aggravate disease progression. After tocilizumab administration, abnormally elevated IL-6, C-reactive protein, fibrinogen, and activated partial thromboplastin time decreased. Tocilizumab may be of value in prolonging survival in patients with severe COVID-19, which provided a novel strategy for COVID-19-induced cytokine release syndrome. Our findings could inform bedside decisions until data from randomized, controlled clinical trials become available.


Subject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , COVID-19/complications , COVID-19/drug therapy , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/drug therapy , Drug Repositioning , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/drug therapy , Aged , COVID-19/immunology , Cohort Studies , Cytokine Release Syndrome/immunology , Female , Humans , Interleukin-6/immunology , Male , Middle Aged , Respiratory Distress Syndrome/immunology , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index
12.
Emerg Microbes Infect ; 9(1): 2571-2577, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-944151

ABSTRACT

Following acute infection, individuals COVID-19 may still shed SARS-CoV-2 RNA. However, limited information is available regarding the active shedding period or whether infectious virus is also shed. Here, we monitored the clinical characteristics and virological features of 38 patients with COVID-19 (long-term carriers) who recovered from the acute disease, but still shed viral RNA for over 3 months. The median carrying history of the long-term carriers was 92 days after the first admission, and the longest carrying history was 118 days. Negative-positive viral RNA-shedding fluctuations were observed. Long-term carriers were mostly elderly people with a history of mild infection. Infectious SARS-CoV-2 was isolated from the sputum, where high level viral RNA was found. All nine full-length genomes of samples obtained in March-April 2020 matched early viral clades circulating in January-February 2020, suggesting that these patients persistently carried SARS-CoV-2 and were not re-infected. IgM and IgG antibodies and neutralizing-antibody profiles were similar between long-term carriers and recovered patients with similar disease courses. In summary, although patients with COVID-19 generated neutralizing antibodies, they may still shed infectious SARS-CoV-2 for over 3 months. These data imply that patients should be monitored after discharge to control future outbreaks.


Subject(s)
COVID-19/virology , SARS-CoV-2/physiology , Virus Shedding , Adult , Aged , Antibodies, Neutralizing , Antibodies, Viral/blood , Carrier State , Female , Genome, Viral , Humans , Immunoglobulin G/blood , Immunoglobulin M/blood , Male , Middle Aged , RNA, Viral/isolation & purification , Sputum/virology
13.
J Asthma ; 59(2): 230-238, 2022 02.
Article in English | MEDLINE | ID: covidwho-922319

ABSTRACT

OBJECTIVE: Although it is reported that patients with coronavirus disease 2019 (COVID-19) disease who have comorbidities are at higher risk to suffer adverse clinical outcomes, there are inadequate evidence to clarify the association between COVID-19 and asthma. On this ground, this study aims to systematically analyze the clinical characteristics of COVID-19 patients with asthma. METHODS: In this single-center, retrospective and observational cohort study, 21 COVID-19 patients with asthma and 100 non-asthma COVID-19 patients were statistically matched by propensity score based on age, sex and comorbidities. Meanwhile, a collection and comparison concerning demographic indicators, clinical and laboratory examinations, treatments and outcomes were conducted between two groups to specify their differences. RESULTS: Statistically, the COVID-19 patients with asthma had a higher proportion of ICU admission (14.3% [3/21] vs. 2.1% [2/96] p = 0.040) than those who do not have. On top this, a higher level of inflammatory responses, such as interleukin 6, interleukin 8, procalcitonin, leukocytes, neutrophils and CD4+ T cells was presented in asthma patients. Moreover, the increase of organ damage indices like D-dimer, lactate dehydrogenase and high-sensitivity cardiac troponin I, were more pronounced in COVID-19 patients with asthma. CONCLUSIONS: Exacerbated inflammatory responses and multiple organ damages were triggered in COVID-19 patients with asthma, which highlights more intensive surveillance and supportive treatment.


Subject(s)
Asthma/epidemiology , COVID-19/epidemiology , COVID-19/physiopathology , Adult , Age Factors , Aged , China/epidemiology , Comorbidity , Female , Humans , Inflammation Mediators/metabolism , Intensive Care Units , Male , Middle Aged , Organ Dysfunction Scores , Retrospective Studies , SARS-CoV-2 , Sex Factors
14.
ERJ Open Res ; 6(2)2020 Apr.
Article in English | MEDLINE | ID: covidwho-853162

ABSTRACT

In response to the early outbreak of SARS-CoV-2, online fever clinics were set up. Then, an online face-to-face consultation was developed to solve the extreme difficulty of getting medical services to patients with chronic diseases. http://bit.ly/3cPppai.

15.
J Med Virol ; 92(7): 807-813, 2020 07.
Article in English | MEDLINE | ID: covidwho-823738

ABSTRACT

In December 2019, an outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection occurred in Wuhan, and rapidly spread to worldwide, which has attracted many people's concerns about the patients. However, studies on the infection status of medical personnel is still lacking. A total of 54 cases of SARS-Cov-2 infected medical staff from Tongji Hospital between 7 January and 11 February 2020 were analyzed in this retrospective study. Clinical and epidemiological characteristics were compared between different groups by statistical method. From 7 January to 11 February 2020, 54 medical staff of Tongji Hospital were hospitalized due to coronavirus disease 2019 (COVID-19). Most of them were from other clinical departments (72.2%) rather than emergency department (3.7%) or medical technology departments (18.5%). Among the 54 patients with COVID-19, the distribution of age had a significant difference between non-severe type and severe/critical cases (median age: 47 years vs 38 years; P = .0015). However, there was no statistical difference in terms of gender distribution and the first symptoms between theses two groups. Furthermore, we observed that the lesion regions in SARS-Cov-2 infected lungs with severe-/critical-type of medical staff were more likely to exhibit lesions in the right upper lobe (31.7% vs 0%; P = .028) and right lung (61% vs 18.2%; P = .012). Based on our findings with medical staff infection data, we suggest training for all hospital staff to prevent infection and preparation of sufficient protection and disinfection materials.


Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/physiopathology , Coronavirus Infections/transmission , Infectious Disease Transmission, Patient-to-Professional/classification , Pneumonia, Viral/physiopathology , Pneumonia, Viral/transmission , Adult , Aged , Anti-Bacterial Agents/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , COVID-19 , China , Coronavirus Infections/diagnosis , Coronavirus Infections/drug therapy , Female , Hospital Departments/classification , Humans , Immunoglobulins/therapeutic use , Interferons/therapeutic use , Male , Medical Staff, Hospital , Middle Aged , Pandemics , Pneumonia, Viral/diagnosis , Pneumonia, Viral/drug therapy , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index , Treatment Outcome
19.
J Med Virol ; 92(11): 2758-2767, 2020 11.
Article in English | MEDLINE | ID: covidwho-599691

ABSTRACT

BACKGROUND: Since the outbreak of 2019 novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) pneumonia, thousands of patients with fever or cough were flocked into fever clinic of designated hospitals in Wuhan, China. To date, no data have ever been reported to reflect the prevalence of coronavirus disease 2019 (COVID-19) among these outpatients. Moreover, it is almost unknown to discriminate COVID-19 and nucleic acid negative patients based on clinical features in the fever clinics. METHODS: The infectious status of SARS-CoV-2 was estimated among the outpatients. The epidemiological and clinical characteristics were compared between COVID-19 and nucleic acid negative patients. RESULTS: The nucleic acid positive rate for SARS-CoV-2 in the outpatients from our fever clinic was 67·1%, while the majority of patients with COVID-19 were mild cases. The predominant initial symptom in those patients with COVID-19 was fever (78.2%), followed by cough (15.6%). Very significantly lower number of eosinophils was characterized in patients with COVID-19 as compared with that of nucleic acid negative patients. More importantly, the proportion of subjects with eosinophil counts lower than normal levels in patients with COVID-19 was much higher than that of nucleic acid negative patients. Fever combined with bilateral ground-glass opacities in computed tomography imaging and eosinophil count below the normal level are probably a valuable indicator of COVID-19 infection in those outpatients. CONCLUSIONS: Those findings may provide critical information for the regions, such as Europe and United States that are facing the same situation as Wuhan experienced, and could be valuable to prevent those nucleic acid negative patients from misdiagnosis before antibody testing.


Subject(s)
COVID-19/epidemiology , Fever/epidemiology , Fever/virology , Outpatients/statistics & numerical data , Adult , Aged , Ambulatory Care Facilities , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19 Nucleic Acid Testing , China/epidemiology , Cough/epidemiology , Eosinophils , Female , Humans , Male , Middle Aged
20.
JCI Insight ; 5(10)2020 05 21.
Article in English | MEDLINE | ID: covidwho-118074

ABSTRACT

BACKGROUNDThe coronavirus disease 2019 (COVID-19), infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a severe outbreak throughout the world. The host immunity of COVID-19 patients is unknown.METHODSThe routine laboratory tests and host immunity in COVID-19 patients with different severity of illness were compared after patient admission.RESULTSA total of 65 SARS-CoV-2-positive patients were classified as having mild (n = 30), severe (n = 20), and extremely severe (n = 15) illness. Many routine laboratory tests, such as ferritin, lactate dehydrogenase, and D-dimer, were increased in severe and extremely severe patients. The absolute numbers of CD4+ T cells, CD8+ T cells, and B cells were gradually decreased with increased severity of illness. The activation markers such as HLA-DR and CD45RO expressed on CD4+ and CD8+ T cells were increased in severe and extremely severe patients compared with mild patients. The costimulatory molecule CD28 had opposite results. The percentage of natural Tregs was decreased in extremely severe patients. The percentage of IFN-γ-producing CD8+ T cells was increased in both severe and extremely severe patients compared with mild patients. The percentage of IFN-γ-producing CD4+ T cells was increased in extremely severe patients. IL-2R, IL-6, and IL-10 were all increased in extremely severe patients. The activation of DC and B cells was decreased in extremely severe patients.CONCLUSIONThe number and function of T cells are inconsistent in COVID-19 patients. The hyperfunction of CD4+ and CD8+ T cells is associated with the pathogenesis of extremely severe SARS-CoV-2 infection.FUNDINGThis work was funded by the National Mega Project on Major Infectious Disease Prevention (2017ZX10103005-007) and the Fundamental Research Funds for the Central Universities (2019kfyRCPY098).


Subject(s)
Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , Betacoronavirus , CD4-Positive T-Lymphocytes/immunology , CD8-Positive T-Lymphocytes/immunology , COVID-19 , Cytokines/metabolism , Diagnostic Tests, Routine , Female , Humans , Immunity , Lymphocyte Count , Male , Middle Aged , Pandemics , SARS-CoV-2 , Severity of Illness Index , T-Lymphocytes/immunology
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