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1.
PLoS One ; 16(4): e0250815, 2021.
Article in English | MEDLINE | ID: covidwho-1833533

ABSTRACT

BACKGROUND: COVID-19 is a respiratory infectious disease caused by SARS-CoV-2, and cardiovascular damage is commonly observed in affected patients. We sought to investigate the effect of SARS-CoV-2 infection on cardiac injury and hypertension during the current coronavirus pandemic. STUDY DESIGN AND METHODS: The clinical data of 366 hospitalized COVID-19-confirmed patients were analyzed. The clinical signs and laboratory findings were extracted from electronic medical records. Two independent, experienced clinicians reviewed and analyzed the data. RESULTS: Cardiac injury was found in 11.19% (30/268) of enrolled patients. 93.33% (28/30) of cardiac injury cases were in the severe group. The laboratory findings indicated that white blood cells, neutrophils, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase were positively associated with cardiac injury marker. Compared with healthy controls, the 190 patients without prior hypertension have higher AngⅡ level, of which 16 (8.42%) patients had a rise in blood pressure to the diagnostic criteria of hypertension during hospitalization, with a significantly increased level of the cTnI, procalcitonin, angiotensin-II (AngⅡ) than those normal blood pressure ones. Multivariate analysis indicated that elevated age, cTnI, the history of hypertension, and diabetes were independent predictors for illness severity. The predictive model, based on the four parameters and gender, has a good ability to identify the clinical severity of COVID-19 in hospitalized patients (area under the curve: 0.932, sensitivity: 98.67%, specificity: 75.68%). CONCLUSION: Hypertension, sometimes accompanied by elevated cTnI, may occur in COVID-19 patients and become a sequela. Enhancing Ang II signaling, driven by SARS-CoV-2 infection, might play an important role in the renin-angiotensin system, and consequently lead to the development of hypertension in COVID-19.


Subject(s)
COVID-19/complications , Heart Injuries/epidemiology , Hypertension/epidemiology , Adult , Aged , Aged, 80 and over , COVID-19/metabolism , COVID-19/physiopathology , Comorbidity , Disease Progression , Female , Heart Injuries/virology , Hospitalization , Humans , Hypertension/physiopathology , Hypertension/virology , Male , Medical Records , Middle Aged , Pandemics , Renin-Angiotensin System , SARS-CoV-2/pathogenicity
2.
Rev Esp Cardiol ; 74(7): 608-615, 2021 Jul.
Article in Spanish | MEDLINE | ID: covidwho-1805063

ABSTRACT

INTRODUCTION AND OBJECTIVES: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2. Atrial fibrillation (AF) is common in acute situations, where it is associated with more complications and higher mortality. METHODS: Analysis of the international HOPE registry (NCT04334291). The objective was to assess the prognostic information of AF in COVID-19 patients. A multivariate analysis and propensity score matching were performed to assess the relationship between AF and mortality. We also evaluated the impact on mortality and embolic events of the CHA2DS2-VASc score in these patients. RESULTS: Among 6217 patients enrolled in the HOPE registry, 250 had AF (4.5%). AF patients had a higher prevalence of cardiovascular risk factors and comorbidities. After propensity score matching, these differences were attenuated. Despite this, patients with AF had a higher incidence of in-hospital complications such as heart failure (19.3% vs 11.6%, P = .021) and respiratory insufficiency (75.9% vs 62.3%, P = .002), as well as a higher 60-day mortality rate (43.4% vs 30.9%, P = .005). On multivariate analysis, AF was independently associated with higher 60-day mortality (hazard ratio, 1.234; 95%CI, 1.003-1.519). CHA2DS2-VASc score acceptably predicts 60-day mortality in COVID-19 patients (area ROC, 0.748; 95%CI, 0.733-0.764), but not its embolic risk (area ROC, 0.411; 95%CI, 0.147-0.675). CONCLUSIONS: AF in COVID-19 patients is associated with a higher number of complications and 60-day mortality. The CHA2DS2-VASc score may be a good risk marker in COVID patients but does not predict their embolic risk.

3.
EClinicalMedicine ; 26: 100527, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-1796940

ABSTRACT

BACKGROUND: Multisystem inflammatory syndrome in children (MIS-C), also known as pediatric inflammatory multisystem syndrome, is a new dangerous childhood disease that is temporally associated with coronavirus disease 2019 (COVID-19). We aimed to describe the typical presentation and outcomes of children diagnosed with this hyperinflammatory condition. METHODS: We conducted a systematic review to communicate the clinical signs and symptoms, laboratory findings, imaging results, and outcomes of individuals with MIS-C. We searched four medical databases to encompass studies characterizing MIS-C from January 1st, 2020 to July 25th, 2020. Two independent authors screened articles, extracted data, and assessed risk of bias. This review was registered with PROSPERO CRD42020191515. FINDINGS: Our search yielded 39 observational studies (n = 662 patients). While 71·0% of children (n = 470) were admitted to the intensive care unit, only 11 deaths (1·7%) were reported. Average length of hospital stay was 7·9 ± 0·6 days. Fever (100%, n = 662), abdominal pain or diarrhea (73·7%, n = 488), and vomiting (68·3%, n = 452) were the most common clinical presentation. Serum inflammatory, coagulative, and cardiac markers were considerably abnormal. Mechanical ventilation and extracorporeal membrane oxygenation were necessary in 22·2% (n = 147) and 4·4% (n = 29) of patients, respectively. An abnormal echocardiograph was observed in 314 of 581 individuals (54·0%) with depressed ejection fraction (45·1%, n = 262 of 581) comprising the most common aberrancy. INTERPRETATION: Multisystem inflammatory syndrome is a new pediatric disease associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that is dangerous and potentially lethal. With prompt recognition and medical attention, most children will survive but the long-term outcomes from this condition are presently unknown. FUNDING: Parker B. Francis and pilot grant from 2R25-HL126140. Funding agencies had no involvement in the study.

4.
Sangyo Eiseigaku Zasshi ; 64(2): 107-113, 2022 Mar 25.
Article in Japanese | MEDLINE | ID: covidwho-1760008

ABSTRACT

OBJECTIVES: Immediately before the state of emergency was declared, there was an outbreak of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) among special training participants with severe physical stress. For promoting the optimization of infection prevention measures by identifying acts and situations with high risk of infection, we conducted a survey and analysis to understand the detailed process of infection spread in these cases. METHODS: A structured interview was conducted for the special training participants on their health status, changes in symptoms, training methods, and behavior history in their private lives. Additionally, a patrol of the training facility was carried out to understand the training environment, and antibody tests were conducted on the close contacts for more accurately grasping the spread of infection, by identifying subclinical infected persons. RESULTS: Within 10 days of COVID-19 onset in the first patient, 15 of the 19 original training participants developed symptoms, and 14 patients tested positive for RT-PCR. PCR tests were also performed on four patients who did not develop the disease - two were positive and negative, each. The two negatives turned positive on a later antibody test, suggesting that there was an asymptomatic infection. In addition, all five patients who participated in the training for only a day developed symptoms and tested positive for PCR in a few days. Of the 64 people who underwent testing for antibodies as close contacts, all but one who was living together with a patient were negative on antibody testing. CONCLUSIONS: The onset of COVID-19 occurred after the start of practice-based training continuously; therefore, the practice-based training was thought to be the main cause of the transmission. We speculate that the main factors behind the rapid spread of infection are as follows: during practice-based training, increased ventilation made it difficult to wear a mask; repeated loud vocalizations at close range; and the training pair was not fixed. Physical training without shouting and desk work, however, did not possess the risk of COVID-19, and avoiding certain situations at high risk of respiratory infections may have significantly reduced SARS-CoV-2 transmission. If personnel become infected with SARS-CoV-2, emergency measures should be devised by identifying patients and close contacts and facilitating the investigation of their behavioral history. Furthermore, evaluating and improving the effectiveness of infection control measures is necessary by ascertaining potentially infected persons by performing PCR tests, antigen tests, antibody tests, etc. in combination.


Subject(s)
COVID-19 , SARS-CoV-2 , COVID-19/epidemiology , Disease Outbreaks/prevention & control , Humans , Inservice Training , Surveys and Questionnaires
5.
QJM ; 114(9): 625-635, 2021 Nov 13.
Article in English | MEDLINE | ID: covidwho-1746245

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been linked to the Guillain-Barré syndrome (GBS). The objective of the present study is to identify specific clinical features of cases of GBS reported in the literature associated with SARS-CoV-2 infection. We searched Pubmed, and included single case reports and case series with full text in English, reporting original data of patients with GBS and a confirmed recent SARS-CoV-2 infection. Clinical data were extracted. We identified 28 articles (22 single case reports and 6 case series), reporting on a total of 44 GBS patients with confirmed SARS-CoV-2 infection. SARS-CoV-2 infection was confirmed through serum reverse transcriptase-polymerase chain reaction in 72.7% of cases. A total of 40 patients (91%) had symptoms compatible with SARS-CoV-2 infection before the onset of the GBS. The median period between the onset of symptoms of SARS-CoV-2 infection and symptoms of the GBS was 11.2 days (range, 2-23). The most common clinical features were: leg weakness (61.4%), leg paresthesia (50%), arm weakness (50.4%), arm paresthesia (50.4%), hyporeflexia/areflexia (48%) and ataxia (22.7%). In total, 38.6% (n = 17) were found to have facial paralysis. Among 37 patients in whom nerve-conduction studies and electromyography were performed, of which 26 patients (59.1%) were consistent with the acute inflammatory demyelinating polyneuropathy subtype of the GBS. The present retrospective analysis support the role of the SARS-CoV-2 infection in the development of the GBS, may trigger GBS as para-infectious disease, and lead to SARS-CoV-2-associated GBS.


Subject(s)
COVID-19 , Communicable Diseases , Guillain-Barre Syndrome , Guillain-Barre Syndrome/complications , Humans , Retrospective Studies , SARS-CoV-2
6.
J Med Virol ; 93(9): 5310-5322, 2021 09.
Article in English | MEDLINE | ID: covidwho-1733920

ABSTRACT

The most consequential challenge raised by coinfection is perhaps the inappropriate generation of recombinant viruses through the exchange of genetic material among different strains. These genetically similar viruses can interfere with the replication process of each other and even compete for the metabolites required for the maintenance of the replication cycle. Due to the similarity in clinical symptoms of most viral respiratory tract infections, and their coincidence with COVID-19, caused by SARS-CoV-2, it is recommended to develop a comprehensive diagnostic panel for detection of respiratory and nonrespiratory viruses through the evaluation of patient samples. Given the resulting changes in blood markers, such as coagulation factors and white blood cell count following virus infection, these markers can be of diagnostic value in the detection of mixed infection in individuals already diagnosed with a certain viral illness. In this review, we seek to investigate the coinfection of SARS-CoV-2 with other respiratory and nonrespiratory viruses to provide novel insights into the development of highly sensitive diagnostics and effective treatment modalities.


Subject(s)
COVID-19/epidemiology , Coinfection , Virus Diseases/epidemiology , Coinfection/epidemiology , Coinfection/virology , Humans
7.
Viruses ; 12(6)2020 06 10.
Article in English | MEDLINE | ID: covidwho-1726021

ABSTRACT

The ongoing Coronavirus Disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) signals an urgent need for an expansion in treatment options. In this study, we investigated the anti-SARS-CoV-2 activities of 22 antiviral agents with known broad-spectrum antiviral activities against coronaviruses and/or other viruses. They were first evaluated in our primary screening in VeroE6 cells and then the most potent anti-SARS-CoV-2 antiviral agents were further evaluated using viral antigen expression, viral load reduction, and plaque reduction assays. In addition to remdesivir, lopinavir, and chloroquine, our primary screening additionally identified types I and II recombinant interferons, 25-hydroxycholesterol, and AM580 as the most potent anti-SARS-CoV-2 agents among the 22 antiviral agents. Betaferon (interferon-ß1b) exhibited the most potent anti-SARS-CoV-2 activity in viral antigen expression, viral load reduction, and plaque reduction assays among the recombinant interferons. The lipogenesis modulators 25-hydroxycholesterol and AM580 exhibited EC50 at low micromolar levels and selectivity indices of >10.0. Combinational use of these host-based antiviral agents with virus-based antivirals to target different processes of the SARS-CoV-2 replication cycle should be evaluated in animal models and/or clinical trials.


Subject(s)
Antiviral Agents/pharmacology , Betacoronavirus/drug effects , Coronavirus Infections/drug therapy , Pneumonia, Viral/drug therapy , Animals , Antigens, Viral/immunology , Betacoronavirus/immunology , Betacoronavirus/metabolism , COVID-19 , Chlorocebus aethiops , Coronavirus Infections/virology , Humans , Interferons/metabolism , Lipogenesis/drug effects , Pandemics , Pneumonia, Viral/virology , SARS-CoV-2 , Signal Transduction/drug effects , Vero Cells , Viral Load/drug effects , Viral Plaque Assay , Virus Replication/drug effects
8.
J Virol ; 94(12)2020 06 01.
Article in English | MEDLINE | ID: covidwho-1723543

ABSTRACT

The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that recently emerged in China is thought to have a bat origin, as its closest known relative (BatCoV RaTG13) was described previously in horseshoe bats. We analyzed the selective events that accompanied the divergence of SARS-CoV-2 from BatCoV RaTG13. To this end, we applied a population genetics-phylogenetics approach, which leverages within-population variation and divergence from an outgroup. Results indicated that most sites in the viral open reading frames (ORFs) evolved under conditions of strong to moderate purifying selection. The most highly constrained sequences corresponded to some nonstructural proteins (nsps) and to the M protein. Conversely, nsp1 and accessory ORFs, particularly ORF8, had a nonnegligible proportion of codons evolving under conditions of very weak purifying selection or close to selective neutrality. Overall, limited evidence of positive selection was detected. The 6 bona fide positively selected sites were located in the N protein, in ORF8, and in nsp1. A signal of positive selection was also detected in the receptor-binding motif (RBM) of the spike protein but most likely resulted from a recombination event that involved the BatCoV RaTG13 sequence. In line with previous data, we suggest that the common ancestor of SARS-CoV-2 and BatCoV RaTG13 encoded/encodes an RBM similar to that observed in SARS-CoV-2 itself and in some pangolin viruses. It is presently unknown whether the common ancestor still exists and, if so, which animals it infects. Our data, however, indicate that divergence of SARS-CoV-2 from BatCoV RaTG13 was accompanied by limited episodes of positive selection, suggesting that the common ancestor of the two viruses was poised for human infection.IMPORTANCE Coronaviruses are dangerous zoonotic pathogens; in the last 2 decades, three coronaviruses have crossed the species barrier and caused human epidemics. One of these is the recently emerged SARS-CoV-2. We investigated how, since its divergence from a closely related bat virus, natural selection shaped the genome of SARS-CoV-2. We found that distinct coding regions in the SARS-CoV-2 genome evolved under conditions of different degrees of constraint and are consequently more or less prone to tolerate amino acid substitutions. In practical terms, the level of constraint provides indications about which proteins/protein regions are better suited as possible targets for the development of antivirals or vaccines. We also detected limited signals of positive selection in three viral ORFs. However, we warn that, in the absence of knowledge about the chain of events that determined the human spillover, these signals should not be necessarily interpreted as evidence of an adaptation to our species.


Subject(s)
Betacoronavirus/genetics , Evolution, Molecular , Selection, Genetic , Amino Acid Sequence , Animals , Betacoronavirus/classification , COVID-19 , Chiroptera/virology , Coronavirus Infections/virology , Genome, Viral/genetics , Humans , Models, Molecular , Open Reading Frames/genetics , Pandemics , Phylogeny , Pneumonia, Viral/virology , SARS-CoV-2 , Viral Proteins/chemistry , Viral Proteins/genetics
9.
Brain Behav Immun ; 87: 34-39, 2020 07.
Article in English | MEDLINE | ID: covidwho-1719335

ABSTRACT

The coronavirus disease 19 (COVID-19) pandemic is a significant psychological stressor in addition to its tremendous impact on every facet of individuals' lives and organizations in virtually all social and economic sectors worldwide. Fear of illness and uncertainty about the future precipitate anxiety- and stress-related disorders, and several groups have rightfully called for the creation and dissemination of robust mental health screening and treatment programs for the general public and front-line healthcare workers. However, in addition to pandemic-associated psychological distress, the direct effects of the virus itself (several acute respiratory syndrome coronavirus; SARS-CoV-2), and the subsequent host immunologic response, on the human central nervous system (CNS) and related outcomes are unknown. We discuss currently available evidence of COVID-19 related neuropsychiatric sequelae while drawing parallels to past viral pandemic-related outcomes. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes, may accompany acute viral infection, or may follow infection by weeks, months, or longer in recovered patients. The potential mechanisms are also discussed, including viral and immunological underpinnings. Therefore, prospective neuropsychiatric monitoring of individuals exposed to SARS-CoV-2 at various points in the life course, as well as their neuroimmune status, are needed to fully understand the long-term impact of COVID-19, and to establish a framework for integrating psychoneuroimmunology into epidemiologic studies of pandemics.


Subject(s)
Coronavirus Infections/psychology , Cytokine Release Syndrome/psychology , Mental Disorders/psychology , Nervous System Diseases/psychology , Pneumonia, Viral/psychology , Acute Disease , Anxiety/etiology , Anxiety/immunology , Anxiety/psychology , Bacterial Translocation , Betacoronavirus , COVID-19 , Chronic Disease , Coronavirus Infections/complications , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/therapy , Demyelinating Diseases/etiology , Demyelinating Diseases/immunology , Demyelinating Diseases/physiopathology , Demyelinating Diseases/psychology , Depression/etiology , Depression/immunology , Depression/psychology , Humans , Immunologic Factors/adverse effects , Mental Disorders/etiology , Mental Disorders/immunology , Mental Health , Nervous System Diseases/etiology , Nervous System Diseases/immunology , Nervous System Diseases/physiopathology , Neurodegenerative Diseases/etiology , Neurodegenerative Diseases/immunology , Neurodegenerative Diseases/physiopathology , Neurodegenerative Diseases/psychology , Pandemics , Pneumonia, Viral/complications , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Psychoneuroimmunology , Psychotic Disorders/etiology , Psychotic Disorders/immunology , Psychotic Disorders/psychology , Public Health , SARS-CoV-2 , Stress Disorders, Post-Traumatic/etiology , Stress Disorders, Post-Traumatic/immunology , Stress Disorders, Post-Traumatic/psychology
11.
J Am Soc Nephrol ; 32(9): 2242-2254, 2021 09.
Article in English | MEDLINE | ID: covidwho-1702796

ABSTRACT

BACKGROUND: Although coronavirus disease 2019 (COVID-19) causes significan t morbidity, mainly from pulmonary involvement, extrapulmonary symptoms are also major componen ts of the disease. Kidney disease, usually presenting as AKI, is particularly severe among patients with COVID-19. It is unknown, however, whether such injury results from direct kidney infection with COVID-19's causative virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), or from indirect mechanisms. METHODS: Using ex vivo cell models, we sought to analyze SARS-CoV-2 interactions with kidney tubular cells and assess direct tubular injury. These models comprised primary human kidney epithelial cells (derived from nephrectomies) and grown as either proliferating monolayers or quiescent three-dimensional kidney spheroids. RESULTS: We demonstrated that viral entry molecules and high baseline levels of type 1 IFN-related molecules were present in monolayers and kidney spheroids. Although both models support viral infection and replication, they did not exhibit a cytopathic effect and cell death, outcomes that were strongly present in SARS-CoV-2-infected controls (African green monkey kidney clone E6 [Vero E6] cultures). A comparison of monolayer and spheroid cultures demonstrated higher infectivity and replication of SARS-CoV-2 in actively proliferating monolayers, although the spheroid cultures exhibited high er levels of ACE2. Monolayers exhibited elevation of some tubular injury molecules-including molecules related to fibrosis (COL1A1 and STAT6) and dedifferentiation (SNAI2)-and a loss of cell identity, evident by reduction in megalin (LRP2). The three-dimensional spheroids were less prone to such injury. CONCLUSIONS: SARS-CoV-2 can infect kidney cells without a cytopathic effect. AKI-induced cellular proliferation may potentially intensify infectivity and tubular damage by SARS-CoV-2, suggesting that early intervention in AKI is warranted to help minimize kidney infection.


Subject(s)
Acute Kidney Injury/etiology , Acute Kidney Injury/virology , COVID-19/complications , SARS-CoV-2/pathogenicity , Spheroids, Cellular/virology , Animals , Cells, Cultured , Chlorocebus aethiops , Cohort Studies , Cytopathogenic Effect, Viral , Epithelial Cells/pathology , Epithelial Cells/virology , Host Microbial Interactions , Humans , Interferon Type I/metabolism , Kidney/immunology , Kidney/pathology , Kidney/virology , Mice , Mice, Inbred NOD , Mice, SCID , Models, Biological , Pandemics , Receptors, Virus/metabolism , Retrospective Studies , SARS-CoV-2/physiology , Spheroids, Cellular/pathology , Vero Cells , Virus Replication
12.
SN Compr Clin Med ; 2(9): 1430-1435, 2020.
Article in English | MEDLINE | ID: covidwho-1682606

ABSTRACT

The current outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) also known as coronavirus disease 2019 (COVID-19) has quickly progressed to a global pandemic. There are well-documented cardiac complications of COVID-19 in patients with and without prior cardiovascular disease. The cardiac complications include myocarditis, heart failure, and acute coronary syndrome resulting from coronary artery thrombosis or SARS-CoV-2-related plaque ruptures. There is growing evidence showing that arrhythmias are also one of the major complications. Myocardial inflammation caused by viral infection leads to electrophysiological and structural remodeling as a possible mechanism for arrhythmia. This could also be the mechanism through which SARS-CoV-2 leads to different arrhythmias. In this review article, we discuss arrhythmia manifestations in COVID-19.

13.
Clin Infect Dis ; 74(2): 294-300, 2022 01 29.
Article in English | MEDLINE | ID: covidwho-1662109

ABSTRACT

BACKGROUND: A better understanding of reinfection after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has become one of the healthcare priorities in the current pandemic. We determined the rate of reinfection, associated factors, and mortality during follow-up in a cohort of patients with SARS-CoV-2 infection. METHODS: We analyzed 9119 patients with SARS-CoV-2 infection who received serial tests in total of 62 healthcare facilities in the United States between 1 December 2019 and 13 November 2020. Reinfection was defined by 2 positive tests separated by interval of >90 days and resolution of first infection was confirmed by 2 or more consecutive negative tests. We performed logistic regression analysis to identify demographic and clinical characteristics associated with reinfection. RESULTS: Reinfection was identified in 0.7% (n = 63, 95% confidence interval [CI]: .5%-.9%) during follow-up of 9119 patients with SARS-CoV-2 infection. The mean period (±standard deviation [SD]) between 2 positive tests was 116 ± 21 days. A logistic regression analysis identified that asthma (odds ratio [OR] 1.9, 95% CI: 1.1-3.2) and nicotine dependence/tobacco use (OR 2.7, 95% CI: 1.6-4.5) were associated with reinfection. There was a significantly lower rate of pneumonia, heart failure, and acute kidney injury observed with reinfection compared with primary infection among the 63 patients with reinfection There were 2 deaths (3.2%) associated with reinfection. CONCLUSIONS: We identified a low rate of reinfection confirmed by laboratory tests in a large cohort of patients with SARS-CoV-2 infection. Although reinfection appeared to be milder than primary infection, there was associated mortality.


Subject(s)
COVID-19 , SARS-CoV-2 , Humans , Pandemics , Reinfection , United States/epidemiology
14.
Br J Nutr ; 127(6): 896-903, 2022 03 28.
Article in English | MEDLINE | ID: covidwho-1651089

ABSTRACT

Coronavirus disease 2019 (COVID-19) has caused mild illness in children, until the emergence of the novel hyperinflammatory condition paediatric inflammatory multisystem syndrome temporally associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (PIMS-TS). PIMS-TS is thought to be a post-SARS-CoV-2 immune dysregulation with excessive inflammatory cytokine release. We studied 25 hydroxyvitamin D (25OHD) concentrations in children with PIMS-TS, admitted to a tertiary paediatric hospital in the UK, due to its postulated role in cytokine regulation and immune response. Eighteen children (median (range) age 8·9 (0·3-14·6) years, male = 10) met the case definition. The majority were of Black, Asian and Minority Ethnic (BAME) origin (89 %, 16/18). Positive SARS-CoV-2 IgG antibodies were present in 94 % (17/18) and RNA by PCR in 6 % (1/18). Seventy-eight percentage of the cohort were vitamin D deficient (< 30 nmol/l). The mean 25OHD concentration was significantly lower when compared with the population mean from the 2015/16 National Diet and Nutrition Survey (children aged 4-10 years) (24 v. 54 nmol/l (95 % CI -38·6, -19·7); P < 0·001). The paediatric intensive care unit (PICU) group had lower mean 25OHD concentrations compared with the non-PICU group, but this was not statistically significant (19·5 v. 31·9 nmol/l; P = 0·11). The higher susceptibility of BAME children to PIMS-TS and also vitamin D deficiency merits contemplation. Whilst any link between vitamin D deficiency and the severity of COVID-19 and related conditions including PIMS-TS requires further evidence, public health measures to improve vitamin D status of the UK BAME population have been long overdue.


Subject(s)
COVID-19 , COVID-19/complications , Child , Child, Preschool , Humans , Male , SARS-CoV-2 , Systemic Inflammatory Response Syndrome , Vitamin D
15.
J Infect Dis ; 2021 Apr 08.
Article in English | MEDLINE | ID: covidwho-1635671

ABSTRACT

Non-pharmaceutical interventions (NPIs) have "flattened the curve" of the COVID-19 pandemic, however the effect of these interventions on other respiratory viruses is unknown. We used aggregate level case count data for eight respiratory viruses and compared the institutional and statewide case counts before and during the period that NPIs were active. We observed a 61% (IRR 0.39, 95% CI 0.37 to 0.41, P < 0.0001) decrease in non-SARS-CoV-2 respiratory viral infections when NPIs were implemented. This finding, if further verified, should guide future public health initiatives to mitigate viral epidemics.

16.
Disaster Med Public Health Prep ; 15(5): e33-e42, 2021 10.
Article in English | MEDLINE | ID: covidwho-1632365

ABSTRACT

OBJECTIVES: An unprecedented wave of patients with acute respiratory failure due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease 2019 (COVID-19) hit emergency departments (EDs) in Lombardy, starting in the second half of February 2020. This study describes the direct and indirect impacts of the SARS-CoV-2 outbreak on an urban major-hospital ED. METHODS: Data regarding all patients diagnosed with COVID-19 presenting from February 1 to March 31, 2020, were prospectively collected, while data regarding non-COVID patients presenting within the same period in 2019 were retrospectively retrieved. RESULTS: ED attendance dropped by 37% in 2020. Two-thirds of this reduction occurred early after the identification of the first autochthonous COVID-19 case in Lombardy, before lockdown measures were enforced. Hospital admissions of non-COVID patients fell by 26%. During the peak of COVID-19 attendance, the ED faced an extraordinary increase in: patients needing oxygen (+239%) or noninvasive ventilation (+725%), transfers to the intensive care unit (+57%), and in-hospital mortality (+309%), compared with the same period in 2019. CONCLUSIONS: The COVID-19 outbreak determined an unprecedented upsurge in respiratory failure cases and mortality. Fear of contagion triggered a spontaneous, marked reduction of ED attendance, and, presumably, some as yet unknown quantity of missed or delayed diagnoses for conditions other than COVID-19.


Subject(s)
COVID-19 , SARS-CoV-2 , Communicable Disease Control , Emergency Service, Hospital , Fear , Humans , Retrospective Studies
17.
Eur J Neurol ; 28(10): 3411-3417, 2021 10.
Article in English | MEDLINE | ID: covidwho-1607226

ABSTRACT

BACKGROUND AND PURPOSE: Since the outbreak of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic, several reports indicated neurological involvement in COVID-19 disease. Muscle involvement has also been reported as evidenced by creatine kinase (CK) elevations and reports of myalgia. METHODS: Creatine kinase, markers of inflammation, pre-existing diseases and statin use were extracted from records of Austrian hospitalised COVID-19 patients. Disease severity was classified as severe in case of intensive care unit (ICU) admission or mortality. COVID-19 patients were additionally compared to an historical group of hospitalised influenza patients. RESULTS: Three hundred fifty-one patients with SARS-CoV-2 and 258 with influenza were included in the final analysis. CK was elevated in 27% of COVID-19 and in 28% of influenza patients. CK was higher in severe COVID-19 as were markers of inflammation. CK correlated significantly with inflammation markers, which had an independent impact on CK when adjusted for demographic variables and disease severity. Compared to influenza patients, COVID-19 patients were older, more frequently male, had more comorbidities, and more frequently had a severe disease course. Nevertheless, influenza patients had higher baseline CK than COVID-19, and 35.7% of intensive care unit (ICU)-admitted patients had CK levels >1,000 U/L compared to only 4.7% of ICU-admitted COVID-19 patients. CONCLUSIONS: HyperCKemia occurs in a similar frequency in COVID-19 and influenza infection. CK levels were lower in COVID-19 than in influenza in mild and severe disease. CK levels strongly correlate with disease severity and markers of inflammation. To date, it remains unclear whether hyperCKemia is due to a virus-triggered inflammatory response or direct muscle toxicity.


Subject(s)
COVID-19 , Influenza, Human , Humans , Influenza, Human/complications , Influenza, Human/epidemiology , Male , Muscles , Pandemics , SARS-CoV-2
18.
Clin Infect Dis ; 73(12): 2283-2293, 2021 12 16.
Article in English | MEDLINE | ID: covidwho-1592629

ABSTRACT

BACKGROUND: Venous thromboembolism (VTE) is a potentially fatal complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and thromboprophylaxis should be balanced against risk of bleeding. This study examined risks of VTE and major bleeding in hospitalized and community-managed SARS-CoV-2 patients compared with control populations. METHODS: Using nationwide population-based registries, 30-day risks of VTE and major bleeding in SARS-CoV-2 positive patients were compared with those of SARS-CoV-2 test-negative patients and with an external cohort of influenza patients. Medical records of all COVID-19 patients at 6 departments of infectious diseases in Denmark were reviewed in detail. RESULTS: The overall 30-day risk of VTE was 0.4% (40/9460) among SARS-CoV-2 patients (16% hospitalized), 0.3% (649/226 510) among SARS-CoV-2 negative subjects (12% hospitalized), and 1.0% (158/16 281) among influenza patients (59% hospitalized). VTE risks were higher and comparable in hospitalized SARS-CoV-2 positive (1.5%), SARS-CoV-2 negative (1.8%), and influenza patients (1.5%). Diagnosis of major bleeding was registered in 0.5% (47/9460) of all SARS-CoV-2 positive individuals and in 2.3% of those hospitalized. Medical record review of 582 hospitalized SARS-CoV-2 patients observed VTE in 4% (19/450) and major bleeding in 0.4% (2/450) of ward patients, of whom 31% received thromboprophylaxis. Among intensive care patients (100% received thromboprophylaxis), risks were 7% (9/132) for VTE and 11% (15/132) for major bleeding. CONCLUSIONS: Among people with SARS-CoV-2 infection in a population-based setting, VTE risks were low to moderate and were not substantially increased compared with SARS-CoV-2 test-negative and influenza patients. Risk of severe bleeding was low for ward patients, but mirrored VTE risk in the intensive care setting.


Subject(s)
COVID-19 , Venous Thromboembolism , Anticoagulants , Cohort Studies , Hemorrhage/epidemiology , Humans , SARS-CoV-2 , Venous Thromboembolism/epidemiology
19.
J Investig Med High Impact Case Rep ; 9: 23247096211013215, 2021.
Article in English | MEDLINE | ID: covidwho-1598539

ABSTRACT

Bronchopleural fistula (BPF) is associated with high morbidity if left untreated. Although rare, the frequency of BPF in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is becoming recognized in medical literature. We present a case of a 64-year-old male with BPF with persistent air leak due to SARS-CoV-2 pneumonia treated with Spiration Valve System endobronchial valve (EBV). An EBV was placed in the right middle lobe with successful cessation of air leak. In conclusion, the use of EBVs for BPF with persistent air leaks in SARS-CoV-2 patients who are poor surgical candidates is effective and safe.


Subject(s)
Bronchial Fistula/surgery , Bronchoscopy , COVID-19/complications , Empyema, Pleural/surgery , Pleural Diseases/surgery , Surgical Instruments , Bronchial Fistula/etiology , Chest Tubes , Empyema, Pleural/etiology , Humans , Male , Middle Aged , Pleural Diseases/etiology , SARS-CoV-2 , Thoracostomy
20.
Signal Transduct Target Ther ; 6(1): 167, 2021 04 24.
Article in English | MEDLINE | ID: covidwho-1585891

ABSTRACT

The ongoing 2019 novel coronavirus disease (COVID-19) caused by SARS-CoV-2 has posed a worldwide pandemic and a major global public health threat. The severity and mortality of COVID-19 are associated with virus-induced dysfunctional inflammatory responses and cytokine storms. However, the interplay between host inflammatory responses and SARS-CoV-2 infection remains largely unknown. Here, we demonstrate that SARS-CoV-2 nucleocapsid (N) protein, the major structural protein of the virion, promotes the virus-triggered activation of NF-κB signaling. After binding to viral RNA, N protein robustly undergoes liquid-liquid phase separation (LLPS), which recruits TAK1 and IKK complex, the key kinases of NF-κB signaling, to enhance NF-κB activation. Moreover, 1,6-hexanediol, the inhibitor of LLPS, can attenuate the phase separation of N protein and restrict its regulatory functions in NF-κB activation. These results suggest that LLPS of N protein provides a platform to induce NF-κB hyper-activation, which could be a potential therapeutic target against COVID-19 severe pneumonia.


Subject(s)
COVID-19/metabolism , Coronavirus Nucleocapsid Proteins/metabolism , NF-kappa B/metabolism , RNA, Viral/metabolism , SARS-CoV-2/metabolism , Signal Transduction , A549 Cells , Acrylates/pharmacology , Animals , COVID-19/drug therapy , COVID-19/pathology , Chlorocebus aethiops , HEK293 Cells , HeLa Cells , Humans , Inflammation/drug therapy , Inflammation/metabolism , Inflammation/pathology , Phosphoproteins/metabolism , Vero Cells
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