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1.
JAMA Neurol ; 79(5): 509-517, 2022 05 01.
Article in English | MEDLINE | ID: covidwho-1729079

ABSTRACT

Importance: Determining the long-term impact of COVID-19 on cognition is important to inform immediate steps in COVID-19 research and health policy. Objective: To investigate the 1-year trajectory of cognitive changes in older COVID-19 survivors. Design, Setting, and Participants: This cohort study recruited 3233 COVID-19 survivors 60 years and older who were discharged from 3 COVID-19-designated hospitals in Wuhan, China, from February 10 to April 10, 2020. Their uninfected spouses (N = 466) were recruited as a control population. Participants with preinfection cognitive impairment, a concomitant neurological disorder, or a family history of dementia were excluded, as well as those with severe cardiac, hepatic, or kidney disease or any kind of tumor. Follow-up monitoring cognitive functioning and decline took place at 6 and 12 months. A total of 1438 COVID-19 survivors and 438 control individuals were included in the final follow-up. COVID-19 was categorized as severe or nonsevere following the American Thoracic Society guidelines. Main Outcomes and Measures: The main outcome was change in cognition 1 year after patient discharge. Cognitive changes during the first and second 6-month follow-up periods were assessed using the Informant Questionnaire on Cognitive Decline in the Elderly and the Telephone Interview of Cognitive Status-40, respectively. Based on the cognitive changes observed during the 2 periods, cognitive trajectories were classified into 4 categories: stable cognition, early-onset cognitive decline, late-onset cognitive decline, and progressive cognitive decline. Multinomial and conditional logistical regression models were used to identify factors associated with risk of cognitive decline. Results: Among the 3233 COVID-19 survivors and 1317 uninfected spouses screened, 1438 participants who were treated for COVID-19 (691 male [48.05%] and 747 female [51.95%]; median [IQR] age, 69 [66-74] years) and 438 uninfected control individuals (222 male [50.68%] and 216 female [49.32%]; median [IQR] age, 67 [66-74] years) completed the 12-month follow-up. The incidence of cognitive impairment in survivors 12 months after discharge was 12.45%. Individuals with severe cases had lower Telephone Interview of Cognitive Status-40 scores than those with nonsevere cases and control individuals at 12 months (median [IQR]: severe, 22.50 [16.00-28.00]; nonsevere, 30.00 [26.00-33.00]; control, 31.00 [26.00-33.00]). Severe COVID-19 was associated with a higher risk of early-onset cognitive decline (odds ratio [OR], 4.87; 95% CI, 3.30-7.20), late-onset cognitive decline (OR, 7.58; 95% CI, 3.58-16.03), and progressive cognitive decline (OR, 19.00; 95% CI, 9.14-39.51), while nonsevere COVID-19 was associated with a higher risk of early-onset cognitive decline (OR, 1.71; 95% CI, 1.30-2.27) when adjusting for age, sex, education level, body mass index, and comorbidities. Conclusions and Relevance: In this cohort study, COVID-19 survival was associated with an increase in risk of longitudinal cognitive decline, highlighting the importance of immediate measures to deal with this challenge.


Subject(s)
COVID-19 , Cognitive Dysfunction , Aged , COVID-19/epidemiology , Cognition , Cognitive Dysfunction/epidemiology , Cognitive Dysfunction/etiology , Cohort Studies , Female , Humans , Longitudinal Studies , Male , SARS-CoV-2 , Survivors
2.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-315710

ABSTRACT

Background: Understanding the long-term effects of coronavirus disease 2019 (COVID-19) on cognitive function is essential for the prevention of cognitive decline in elderly population. This study aims to assess cognitive status and longitudinal decline at 6 months post-infection in elderly patients recovered from COVID-19.Methods: This cross-sectional study recruited 1013 COVID-19 inpatients aged over 60 years who were discharged from three COVID-19-designated hospitals in Wuhan, China, from February 10 to March 13, 2020. In total, 262 uninfected living spouses of COVID-19 patients were selected as controls. Subjects were examined for their current cognitive status using a Chinese version of the Telephone Interview of Cognitive Status-40 (TICS-40) and longitudinal cognitive decline using an Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Cognitive assessments were performed 6 months after patient discharge.Findings: COVID-19 patients had significantly lower TICS-40 scores (patients: 29.73±6.13;controls: 30.74±5.95, p=0.016) and higher IQCODE scores (patients: 3.40±0.81;controls: 3.15±0.39, p<0.001) than the controls. Severe COVID-19 patients had lower TICS-40 scores and higher IQCODE scores than non-severe COVID-19 patients (TICS-40: 22.98±7.12 vs. 30.46±5.53, p<0.001;IQCODE: 4.06±1.39 vs. 3.33±0.68, p<0.001) and controls (TICS-40: 22.98±7.12 vs. 30.74±5.95, p<0.001;IQCODE: 4.06±1.39 vs. 3.15±0.39, p<0.001). Severe COVID-19 patients had a higher proportion of cases with a current cognitive impairment and longitudinal cognitive decline than non-severe COVID-19 patients and controls. COVID-19 severity (OR: 8.142, 95% CI: 5.007-13.239) was associated with worse current cognitive function. Older age (OR: 1.024, 95% CI: 1.003 to 1.046), COVID-19 severity (OR: 2.277, 95% CI: 1.308 to 3.964), mechanical ventilation (OR: 5.388, 95% CI: 3.007 to 9.656), and hypertension (OR: 1.866, 95% CI: 1.376 to 2.531) were associated with an increased risk of longitudinal cognitive decline.Interpretation: SARS-CoV-2 infection is associated with delayed cognitive decline in elderly population. COVID-19 patients with risk factors, including severe disease, older age, mechanical ventilation, and hypertension, should be intensively monitored for delayed cognitive decline. Funding: National Natural Science Foundation of China.Conflict of Interest: We declared no conflict of interests.Ethical Approval: The study protocols were approved by the institutional review boards of the hospitals. Verbal informed consent was obtained from all participants prior to the survey.

3.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-313349

ABSTRACT

Background: Bedside lung ultrasound (LUS) has emerged as a useful and noninvasive tool to detect lung involvement and monitor changes in patients with coronavirus disease 2019 (COVID-19). However, the clinical significance of the LUS score in patients with COVID-19 remains unknown. We aimed to investigate the prognostic value of the LUS score in patients with COVID-19. Methods: : The LUS protocol consisted of 12 scanning zones and was performed in 280 consecutive patients with COVID-19. The LUS score based on B-lines, lung consolidation and pleural line abnormalities was evaluated. Results: : The median time from admission to LUS examinations was 7 days (interquartile range [IQR] 3-10). Patients in the highest LUS score group were more likely to have a lower lymphocyte percentage (LYM%);higher levels of D-dimer, C-reactive protein, hypersensitive troponin I and creatine kinase muscle-brain;more invasive mechanical ventilation therapy;higher incidence of ARDS;and higher mortality than patients in the lowest LUS score group. After a median follow-up of 14 days [IQR, 10-20 days], 37 patients developed ARDS, and 13 died. Patients with adverse outcomes presented a higher rate of bilateral involvement;more involved zones and B-lines, pleural line abnormalities and consolidation;and a higher LUS score than event-free survivors. The Cox models adding the LUS score as a continuous variable (hazard ratio [HR]: 1.05, 95% confidence intervals [CI]: 1.02~1.08;P < 0.001;Akaike Information Criterion [AIC] =272;C-index = 0.903) or as a categorical variable (HR: 10.76, 95% CI: 2.75~42.05;P = 0.001;AIC =272;C-index = 0.902) were found to predict poor outcomes more accurately than the basic model (AIC =286;C-index = 0.866). An LUS score cut-off >12 predicted adverse outcomes with a specificity and sensitivity of 90.5% and 91.9%, respectively. Conclusions: : The LUS score devised by our group performs well at predicting adverse outcomes in patients with COVID-19 and is important for risk stratification in COVID-19 patients.

4.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-324309

ABSTRACT

Background: The coronavirus disease 2019 (COVID-19) is a newly recognized illness that has spread rapidly all over the world. Severe hypoxemic respiratory failure from COVID-19 will bring high risk of venous thromboembolism (VTE). Our study aims to identify in-hospital VTE risk and bleeding risk in COVID-19 patients. Methods We retrospectively studied 138 consecutively enrolled patients with COVID-19 and identified in-hospital VTE and bleeding risk by Padua Prediction Score and Improve bleed risk assessment model. The clinical data and features were analyzed in VTE patients. Results Our findings identified that 23 (16.67%) patients with COVID-19 were at high risk for VTE according to Padua prediction score, and 9(6.52%) patients were at high risk of bleeding for VTE prophylaxis according to Improve prediction score. Fifteen critically ill patients faced double high risk from thrombosis (Padua score more than 4 points in all 15[100%] patients) and hemorrhage (Improve score more than 7 points in 9[60.0%] patients). Thrombotic events were identified in four patients (2.9%) of all COVID-19 patients. All of them were diagnosed as deep vein thrombosis by ultrasound after 3 to 18 days after admission. Three (75.0%) were critically ill patients, which means the incidence of VTE among critically ill patients was 20%. One major hemorrhage was happened in critically ill patients during VTE treatment. Conclusion Critically ill patients with COVID-19 suffered both high risk of thrombosis and bleeding risks. More effective VTE prevention strategies based on an individual assessment of bleeding risks were necessary for critically ill patients with COVID-19.

5.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-323773

ABSTRACT

SARS-CoV-2 has caused the COVID-19 pandemic. Recently, B.1.617 variants have been transmitted rapidly in India. The transmissibility, pathogenicity, and neutralization characteristics of these variants have received considerable interest. In this study, 22 pseudotyped viruses were constructed for B.1.617 variants and their corresponding single amino acid mutations. B.1.617 variants did not exhibit significant enhanced infectivity in human cells, but mutations T478K and E484Q in the receptor binding domain led to enhanced infectivity in mouse ACE2-overexpressing cells. Furin activities were slightly increased against B.1.617 variants and cell–cell fusion after infection of B.1.617 variants was enhanced. Furthermore, B.1.617 variants escaped neutralization by several mAbs, mainly because of mutations L452R, T478K, and E484Q in the receptor binding domain. The neutralization activities of sera from convalescent patients, inactivated vaccine-immunized volunteers, adenovirus vaccine-immunized volunteers, and SARS-CoV-2 immunized animals against pseudotyped B.1.617 variants were reduced by approximately twofold, compared with the D614G variant.

6.
Journal of Applied Virology ; 9(4):41-45, 2020.
Article in English | GIM | ID: covidwho-1344634

ABSTRACT

The dominant N501Y mutation in the spike protein that SARS-CoV-2 virus uses to bind to the human ACE2 receptor were found in the UK, which has aroused global concern and worried. Mutations in spike protein may, in theory, result in more infectious and spreading more easily. In order to evaluate the broad-spectrum protective effect of the monoclonal antibodies(mAbs), we compared the neutralization activities of six prepared mAbs against SARS-CoV-2 with pseudovirus neutralization assay. Only one of them showed a decrease of 6 folds in neutralizing activity to N501Y mutant strain, compared with the wild type strain. We should continue to monitor emergence of new variants in different regions to study their infectivity and neutralization effect.

7.
Mol Neurodegener ; 16(1): 48, 2021 07 19.
Article in English | MEDLINE | ID: covidwho-1318288

ABSTRACT

BACKGROUND: Understanding the long-term effects of coronavirus disease 2019 (COVID-19) on cognitive function is essential for monitoring the cognitive decline in the elderly population. This study aims to assess the current cognitive status and the longitudinal cognitive decline in elderly patients recovered from COVID-19. METHODS: This cross-sectional study recruited 1539 COVID-19 inpatients aged over 60 years who were discharged from three COVID-19-designated hospitals in Wuhan, China, from February 10 to April 10, 2020. In total, 466 uninfected spouses of COVID-19 patients were selected as controls. The current cognitive status was assessed using a Chinese version of the Telephone Interview of Cognitive Status-40 (TICS-40) and the longitudinal cognitive decline was assessed using an Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Cognitive assessments were performed 6 months after patient discharge. RESULTS: Compared with controls, COVID-19 patients had lower TICS-40 scores and higher IQCODE scores [TICS-40 median (IQR): 29 (25 to 32) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR): 3.19 (3.00 to 3.63) vs. 3.06 (3.00 to 3.38), p < 0.001]. Severe COVID-19 patients had lower TICS-40 scores and higher IQCODE scores than non-severe COVID-19 patients [TICS-40 median (IQR): 24 (18 to 28) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR): 3.63 (3.13 to 4.31) vs. 3.13 (3.00 to 3.56), p < 0.001] and controls [TICS-40 median (IQR): 24 (18 to 28) vs. 30 (26 to 33), p < 0.001; IQCODE median (IQR) 3.63 (3.13 to 4.31) vs. 3.06 (3.00 to 3.38), p < 0.001]. Severe COVID-19 patients had a higher proportion of cases with current cognitive impairment and longitudinal cognitive decline than non-severe COVID-19 patients [dementia: 25 (10.50 %) vs. 9 (0.69 %), p < 0.001; Mild cognitive impairment (MCI): 60 (25.21 %) vs. 63 (4.84 %), p < 0.001] and controls [dementia: 25 (10.50 %) vs. 0 (0 %), p < 0.001; MCI: 60 (25.21 %) vs. 20 (4.29 %), p < 0.001)]. COVID-19 severity, delirium and COPD were risk factors of current cognitive impairment. Low education level, severe COVID-19, delirium, hypertension and COPD were risk factors of longitudinal cognitive decline. CONCLUSIONS: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with an increased risk of long-term cognitive decline in elderly population. COVID-19 patients, especially severe patients, should be intensively monitored for post-infection cognitive decline.


Subject(s)
COVID-19/complications , Cognitive Dysfunction/virology , Aged , Aged, 80 and over , COVID-19/epidemiology , China , Cognitive Dysfunction/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , SARS-CoV-2
8.
Eur Neurol ; 83(6): 630-635, 2020.
Article in English | MEDLINE | ID: covidwho-992126

ABSTRACT

Coronavirus disease-2019 (COVID-19) has become a pandemic disease globally. The First Affiliated Hospital of Chengdu Medical College has adopted telestroke to make stroke care accessible in remote areas. During the period January 2020 to March 2020, there was no COVID-19 case reported in our stroke center. A significant reduction of stroke admission was observed between the ischemic stroke group (235 vs. 588 cases) and the intracerebral hemorrhage group (136 vs. 150 cases) when compared with the same period last year (p < 0.001). The mean door-to-needle time (DNT) and door-to-puncture time (DPT) was 62 and 124 min, respectively. Compared to the same period last year, a significant change was observed in DNT (62 ± 12 vs. 47 ± 8 min, p = 0.019) but not in DPT (124 ± 58 vs. 135 ± 23 min, p = 0.682). A total of 46 telestroke consultations were received from network hospitals. Telestroke management in the central hospital was performed on 17 patients. Of them, 3 (17.6%) patients had brain hernia and died in hospital and 8 (47.1%) patients were able to ambulation at discharge and had a modified Rankin Scale of 0-2 at 3 months. The COVID-19 pandemic impacted stroke care significantly in our hospital, including prehospital and in-hospital settings, resulting in a significant drop in acute ischemic stroke admissions and a delay in DNT. The construction of a telestroke network enabled us to extend health-care resources and make stroke care accessible in remote areas. Stroke education and public awareness should be reinforced during the COVID-19 pandemic.


Subject(s)
COVID-19 , Hemorrhagic Stroke/therapy , Ischemic Stroke/therapy , Telemedicine/methods , Thrombectomy/statistics & numerical data , Thrombolytic Therapy/statistics & numerical data , Time-to-Treatment/statistics & numerical data , Aged , Aged, 80 and over , Female , Functional Status , Hospitalization , Hospitals , Humans , Male , Middle Aged , Multi-Institutional Systems/organization & administration , Pandemics , SARS-CoV-2 , Stroke/epidemiology , Telemedicine/organization & administration , Treatment Outcome
9.
Front Immunol ; 11: 585647, 2020.
Article in English | MEDLINE | ID: covidwho-874483

ABSTRACT

Cytokine storm resulting from SARS-CoV-2 infection is one of the leading causes of acute respiratory distress syndrome (ARDS) and lung fibrosis. We investigated the effect of inflammatory molecules to identify any marker that is related to lung fibrosis in coronavirus disease 2019 (COVID-19). Seventy-six COVID-19 patients who were admitted to Youan Hospital between January 21 and March 20, 2020 and recovered were recruited for this study. Pulmonary fibrosis, represented as fibrotic volume on chest CT images, was computed by an artificial intelligence (AI)-assisted program. Plasma samples were collected from the participants shortly after admission, to measure the basal inflammatory molecules levels. At discharge, fibrosis was present in 46 (60.5%) patients whose plasma interferon-γ (IFN-γ) levels were twofold lower than those without fibrosis (p > 0.05). The multivariate-adjusted logistic regression analysis demonstrated the inverse association risk of having lung fibrosis and basal circulating IFN-γ levels with an estimate of 0.43 (p = 0.02). Per the 1-SD increase of basal IFN-γ level in circulation, the fibrosis volume decreased by 0.070% (p = 0.04) at the discharge of participants. The basal circulating IFN-γ levels were comparable with c-reactive protein in the discrimination of the occurrence of lung fibrosis among COVID-19 patients at discharge, unlike circulating IL-6 levels. In conclusion, these data indicate that decreased circulating IFN-γ is a risk factor of lung fibrosis in COVID-19.


Subject(s)
Coronavirus Infections/complications , Interferon-gamma/blood , Pneumonia, Viral/complications , Pulmonary Fibrosis/etiology , Aged , Artificial Intelligence , Biomarkers/blood , COVID-19 , Cohort Studies , Coronavirus Infections/blood , Coronavirus Infections/diagnostic imaging , Coronavirus Infections/immunology , Cross-Sectional Studies , Female , Humans , Inflammation/immunology , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/diagnostic imaging , Pneumonia, Viral/immunology , Pulmonary Fibrosis/blood , Pulmonary Fibrosis/diagnostic imaging , Risk Factors , Tomography, X-Ray Computed
12.
Chin Med ; 15: 78, 2020.
Article in English | MEDLINE | ID: covidwho-688856

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a new global public health emergency. The therapeutic benefits of Cold‒Damp Plague Formula (CDPF) against COVID-19, which was used to treat "cold‒dampness stagnation in the lung" in Trial Versions 6 and 7 of the "Diagnosis and Treatment Protocol for COVID-19", have been demonstrated, but the effective components and their mechanism of action remain unclear. METHODS: In this study, a network pharmacology approach was employed, including drug-likeness evaluation, oral bioavailability prediction, protein‒protein interaction (PPI) network construction and analysis, Gene Ontology (GO) terms, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation, and virtual docking, to predict the bioactive components, potential targets, and molecular mechanism of CDPF for COVID-19 treatment. RESULTS: The active compound of herbs in CDPF and their candidate targets were obtained through database mining, and an herbs-ingredients-targets network was constructed. Subsequently, the candidate targets of the active compounds were compared to those relevant to COVID-19, to identify the potential targets of CDPF for COVID-19 treatment. Subsequently, the PPI network was constructed, which provided a basis for cluster analysis and hub gene screening. The seed targets in the most significant module were selected for further functional annotation. GO enrichment analysis identified four main areas: (1) cellular responses to external stimuli, (2) regulation of blood production and circulation, (3) free radical regulation, (4) immune regulation and anti-inflammatory effects. KEGG pathway analysis also revealed that CDPF could play pharmacological roles against COVID-19 through "multi components‒multi targets‒multi pathways" at the molecular level, mainly involving anti-viral, immune-regulatory, and anti-inflammatory pathways; consequently, a "CDPF-herbs-ingredients-targets-pathways-COVID-19" network was constructed. In hub target analysis, the top hub target IL6, and ACE2, the receptor via which SARS-CoV-2 typically enters host cells, were selected for molecular docking analyses, and revealed good binding activities. CONCLUSIONS: This study revealed the active ingredients and potential molecular mechanism by which CDPF treatment is effective against COVID-19, and provides a reference basis for the wider application and further mechanistic investigations of CDPF in the fight against COVID-19.

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