Corpus overview


Overview

MeSH Disease

Human Phenotype

Pneumonia (130)

Fever (96)

Cough (74)

Severe infection (40)

Fatigue (31)


Transmission

Seroprevalence
    displaying 1 - 10 records in total 781
    records per page




    SARS-CoV-2 S Protein Binding hACE2: Viral Entry, Pathogenesis, Prognosis, and Potential Therapeutic Targets

    Authors: Lobna Al-Zaidan; Sarra Mestiri; Afsheen Raza; Maysaloun Merhi; Varghese Inchakalody; Queenie Fernandez; Nassiba Taib; Shahab Uddin; Said Dermime

    id:10.20944/preprints202009.0420.v1 Date: 2020-09-18 Source: Preprints.org

    Pneumonia HP cases of unknown etiology in Wuhan, China, were reported to the WHO on 31st of December 2019. Later the pathogen was reported to be a novel coronavirus designated Severe Acute Respiratory Syndrome Coronavirus 2 MESHD (SARS-CoV-2) that causes Coronavirus Disease MESHD 2019 (COVID-19). SARS-CoV-2 is a novel pathogenic beta coronavirus that infects MESHD humans causing severe respiratory illness MESHD. However, multifarious factors can contribute to the susceptibility to COVID-19 related morbidity and mortality such as age TRANS, gender TRANS and underlying comorbidities. Importantly, SARS-CoV and SARS-CoV-2 MESHD entry into the host cells is mediated via ACE2 receptor. However, ACE2 receptor binding affinity to SARS-CoV-2 is 4 folds higher than that to SARS-CoV MESHD. Identification of different aspects such as binding affinity, differential antigenic profiles of spike glycoproteins, and ACE2 polymorphisms might influence the investigation of potential therapeutic strategies targeting SARS-CoV-2/ACE2 binding interface. Here we aim to elaborate on SARS-CoV-2 S1/ACE2 ligand that facilitates viral internalization as well as to highlight the differences between SARS-CoVs binding affinity to ACE2. We also discuss the possible immunogenic sequences of spike glycoprotein and the effect of ACE2 polymorphism on viral binding/infectivity and host susceptibility to disease. Furthermore, targeting of ACE2 will be discussed to understand its role in therapeutics.

    The impact of vital signs on the death of patients with new coronavirus pneumonia MESHD pneumonia HP: A systematic review and meta-analysis

    Authors: Meixia Du; Jie Zhao; Xiaochun Yin; Nadi Zhang; Guisen Zheng; Jose Guillermo Gonzalez-Valdez; Rocio Ortiz-Lopez; Augusto Rojas-Martinez; Grissel Trujillo-de Santiago; Mario Moises Alvarez; Jacques Demongeot; Renaud Piarroux; Stanislas Rebaudet; Omai B Garner; Yi Yin; Joshua S Bloom; Leonid Kruglyak; Jason M Goldstein; Joel M Montgomery; Christina F Spiropoulou

    doi:10.1101/2020.09.17.20196709 Date: 2020-09-18 Source: medRxiv

    Background: Assessing the impact of vital signs ( blood SERO pressure, body temperature, heart rate, respiratory rate, and oxygen saturation) on the death of patients with new coronavirus pneumonia MESHD pneumonia HP would provide a simple and convenient method for the monitoring of subsequent illness, and therefore, in some degree reduce treatment costs and increase the cure rate clinically. Methods: Six databases were retrieved. The software R 3.6.2 was used for meta-analysis of the included literature. Results: 12 studies were included, which comprise 8996 patients affected with COVID-19 infection MESHD. The meta-analysis study found that blood SERO pressure (MAP, SBP and DBP), heart rate, respiration rate and SpO2 are the risk factors for disease progression in patients with COVID-19. Among them, the increase in MAP and the decrease in SpO2 have the greatest impact on the death of patients with COVID-19 [MAP: MD = 5.66, 95% CI (0.34, 10.98), SpO2: MD = -5.87, 95% CI (-9.17, -2.57), P = 0.0005]. However, comparing the body temperature of the death group and the survival group found that the body temperature was not statistically significant between the two groups [body temperature: MD = 0.21, 95% CI (-0.01, 0.43), P = 0.0661]. Conclusion: The increase in MAP, heart rate and respiratory rate, as well as the decrease in SBP, DBP and SpO2 are all independent risk factors for death MESHD in patients with COVID-19. These factors are simple and easy to monitor, and individualized treatment can be given to patients in time, reducing the mortality rate and improving treatment efficiency.

    Proteomics identifies a type I IFN, prothrombotic hyperinflammatory circulating COVID-19 neutrophil signature distinct from non-COVID-19 ARDS

    Authors: Leila Reyes; Manuel Alejandro Sanchez-Garcia; Tyler Morrison; Andrew JM Howden; Emily R Watts; Simone Arienti; Pranvera Sadiku; Patricia Coelho; Ananda S Mirchandani; David Hope; Sarah K Clark; Jo Singleton; Shonna Johnston; Robert Grecian; Azin Poon; Sarah McNamara; Isla Harper; Max Head Fourman; Alejandro J Brenes; Shalini Pathak; Amy Lloyd; Gio Rodriguez Blanco; Alex Von Kriegsheim; Bart Ghesquiere; Wesley Vermaelen; Camila T Cologna; Kevin Dhaliwal; Nik Hirani; David Dockrell; Moira KB Whyte; David M Griffith; Doreen A Cantrell; Sarah R Walmsley; Marc P. Hoeppner; Simon Imm; Ralf Juenker; Sina Kaiser; Ying H. Kan; Rainer Knoll; Christoph Lange; Georg Laue; Clemes Lier; Matthias Lindner; Georgios Marinos; Robert Markewitz; Jacob Nattermann; Rainer Noth; Peter Pickkers; Klaus F. Rabe; Alina Renz; Christoph Roecken; Jan Rupp; Annika Schaffarzyk; Alexander Scheffold; Jonas Schulte-Schrepping; Domagoj Schunck; Dirk Skowasch; Thomas Ulas; Klaus-Peter Wandinger; Michael Wittig; Johannes Zimmermann; Hauke Busch; Bimba F. Hoyer; Christoph Kaleta; Jan Heyckendorf; Matthijs Kox; Jan Rybniker; Stefan Schreiber; Joachim Schultze; Philip Rosenstiel; - HCA Lung Biological Network; - Deutsche COVID-19 Omics Initiative (DeCOI)

    doi:10.1101/2020.09.15.20195305 Date: 2020-09-18 Source: medRxiv

    Understanding the mechanisms by which infection with SARS-CoV-2 leads to acute respiratory distress HP respiratory distress MESHD syndrome ( ARDS MESHD) is of significant clinical interest given the mortality associated with severe and critical coronavirus induced disease MESHD 2019 (COVID-19). Neutrophils play a key role in the lung injury MESHD characteristic of non-COVID-19 ARDS, but a relative paucity of these cells is observed at post-mortem in lung tissue of patients who succumb to infection MESHD with SARS-CoV-2. With emerging evidence of a dysregulated innate immune response in COVID-19, we undertook a functional proteomic survey of circulating neutrophil populations, comparing patients with COVID-19 ARDS, non-COVID-19 ARDS, moderate COVID-19, and healthy controls. We observe that expansion of the circulating neutrophil compartment and the presence of activated low and normal density mature and immature neutrophil populations occurs in both COVID-19 and non-COVID-19 ARDS. In contrast, release of neutrophil granule proteins, neutrophil activation of the clotting cascade and formation of neutrophil platelet aggregates is significantly increased in COVID-19 ARDS. Importantly, activation of components of the neutrophil type I IFN responses is specific to infection with SARS-CoV-2 and linked to metabolic rewiring. Together this work highlights how differential activation of circulating neutrophil populations may contribute to the pathogenesis of ARDS, identifying processes that are specific to COVID-19 ARDS.

    Respiratory Rehabilitation After Blood SERO Transfusion in a COVID-19 Patient: A Case Report

    Authors: Mohammad Javad Mousavi; Narges Obeidi; Saeed keshmiri; Farzan Azodi; Jamile Kiyani; Farhad Abbasi

    doi:10.21203/rs.3.rs-78131/v1 Date: 2020-09-15 Source: ResearchSquare

    Background: The coronavirus disease MESHD 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), has been identified as the most crucial threat of the century. Due to severe pneumonia HP pneumonia MESHD and acute respiratory distress syndrome MESHD respiratory distress HP syndrome ( ARDS MESHD), the SARS-CoV-2 can cause shortness of breath MESHD, hypoxemia HP hypoxemia MESHD, and the need to mechanical ventilation, intensive care unit (ICU) management, and eventual death MESHD. We have tried to use a non-invasive approach to prevent patient from needing respiratory support with invasive ventilation (IV). Here, for the first time, improvement of oxygen delivery and oxygen saturation levels were observed in a COVID-19 patient using packed red blood SERO cells (PRBCs) transfusion.Case presentation: A 63-year-old man with a history of smoking and addiction who came to our hospital facility with fever HP fever MESHD, shortness of breath MESHD and decreased blood SERO oxygen saturation. High-resolution chest CT revealed bilateral and multifocal ground-glass opacities consistent with COVID-19. Subsequently, the COVID-19 infection was confirmed TRANS infection was confirmed MESHD by real-time polymerase chain reaction (qRT-PCR) assay of the upper respiratory tract. Conclusions: Oxygen delivery and oxygen saturation improvement were observed in the COVID-19 patient, after PRBCs transfusions.

    A fractional order approach to modeling and simulations of the novel COVID-19

    Authors: Isaac Owusu-Mensah; Lanre Akinyemi; Bismark Oduro; Olaniyi S. Iyiola

    doi:10.21203/rs.3.rs-77269/v1 Date: 2020-09-14 Source: ResearchSquare

    The novel coronavirus (SARS-CoV-2.) has emerged and spread at fast speed globally; the disease has become an unprecedented threat to public health worldwide. It is one of the greatest public health challenges in modern times, with no proven cure or vaccine. In this paper, our focus is on a fractional order approach to modeling and simulations of the novel COVID-19. We introduce a fractional type Susceptible-Exposed-Infected-Recovered (SEIR) model to gain insight into the ongoing pandemic of COVID-19. Our proposed model incorporates transmission TRANS rate, testing rates, and transition rate (from asymptomatic TRANS to symptomatic population groups) for a holistic study of the coronavirus disease MESHD. The impacts of these parameters on the dynamics of the solution proles for the disease are simulated and discussed in detail. Furthermore, across all the different parameters, the effects of the fractional order derivative are also simulated and discussed in detail. Various simulations carried out enable us gain deep insights into the dynamics of the spread of COVID-19. The simulation results confirm that fractional calculus is an appropriate tool in modeling the spread of a complex infectious disease MESHD such as the novel COVID-19. In the absence of vaccine and treatment, our analysis strongly supports the significance reduction in the transmission TRANS rate as valuable strategy to curb the spread of the virus. Our results suggest that tracing TRANS and moving testing up has an important benefit. It reduces the number of infected individuals in the general public and thereby reduce the spread of the pandemic. Once the infected MESHD individuals are identified and isolated, the interaction between susceptible and infected individuals diminishes and transmission TRANS reduces. Furthermore, aggressive testing is also highly recommended.

    COVID-19 outbreak and control in Kenya- Insights from a mathematical model

    Authors: Rachel Waema Mbogo; Titus Okellow Orwa

    doi:10.21203/rs.3.rs-77507/v1 Date: 2020-09-14 Source: ResearchSquare

    The coronavirus disease MESHD 2019 ( COVID -19) pandemic reached Kenya in March 2020 with the initial cases reported in the capital city Nairobi and in the coastal area Mombasa. As reported by the World Health Organization, the outbreak of COVID -19 has spread across the world, killed many, collapsed economies and changed the way people live since it was first reported in Wuhan, China, in the end of 2019. As of May 25,2020 It had led to over 100,000 confirmed cases TRANS in Africa with over 3000 deaths. The trend poses a huge threat to global public health. Understanding the early transmission TRANS dynamics of the infection MESHD and evaluating the effectiveness of control measures is crucial for assessing the potential for sustained transmission TRANS to occur in new areas. We employed a SEIHCRD mathematical transmission TRANS model with reported Kenyan data on cases of COVID -19 to estimate how transmission TRANS varies over time. The model is concise in structure, and successfully captures the course of the COVID -19 outbreak, and thus sheds light on understanding the trends of the outbreak. The next generation matrix approach was adopted to calculate the basic reproduction number TRANS ( $ R_0 TRANS$ ) from the model to assess the factors driving the infection . The results from the model analysis shows that non-pharmaceutical interventions over a relatively long period is needed to effectively get rid of the COVID -19 epidemic otherwise the rate of infection will continue to increase despite the increased rate of recovery.

    Daytime variation in SARS-CoV-2 infection MESHD and cytokine production

    Authors: Aissatou Bailo Diallo; Laetitia Gay; Benjamin Coiffard; Marc Leone; Soraya Mezouar; Jean-Louis Mège; Elisa Ghelfi; Chhinder Sodhi; David Hackam; Lester Kobzik; Ben Croker; Douglas Brownfield; Hongpeng Jia; Kristopher A. Sarosiek; Paige D. Hall; Maud Jansen; Kumaran Shanmugarajah; Jessica S. Donington; Florian Krammer; Daved Fremont; Andrzej Joachimiak; Yoshihiro Kawaoka; Vera Tesic; Maria Lucia Madariaga; Patrick C Wilson; Martin Pettersson; Mattew R. Reese; Thomas Rogers; Michelle I Rossulek; Jean G Sathish; Claire Steppan; Martyn Ticehurst; Lawrence W. Updyke; Yuao Zhu; Jun Wang; Arnab K Chatterjee; Andrew D Mesecar; Annaliesa S. Anderson; Charlotte Allerton

    doi:10.1101/2020.09.09.290718 Date: 2020-09-12 Source: bioRxiv

    S. Ray and A. Reddy recently anticipated the implication of circadian rhythm in severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), which is the causative agent of the coronavirus disease MESHD (Covid-19). In addition to its key role in the regulation of biological functions, the circadian rhythm has been suggested as a regulator of viral infections MESHD. Specifically, the time of day of infection MESHD was found critical for illness progression, as has been reported for influenza, respiratory syncytial and parainfluenza type 3 viruses. We analyzed circadian rhythm implication in SARS-CoV-2 virus infection MESHD of isolated human monocytes, key actor cells in Covid-19 disease, from healthy subjects. The circadian gene expression of Bmal1 and Clock genes was investigated with q-RTPCR. Monocytes were infected with SARS-CoV-2 virus strain and viral infection MESHD was investigated by One-Step qRT-PCR and immunofluorescence. Interleukin (IL)-6, IL-1{beta} and IL-10 levels were also measured in supernatants of infected monocytes. Using Cosinor analysis, we showed that Bmal1 and Clock transcripts exhibited circadian rhythm in monocytes with an acrophase and a bathyphase at Zeitgeber Time (ZT)6 and ZT17. After forty-eight hours, the amount of SARS-CoV-2 virus increased in the monocyte infected at ZT6 compared to ZT17. The high virus amount at ZT6 was associated with significant increased release in IL-6, IL-1{beta} and IL-10 compared to ZT17. Our results suggest that time day of SARS-CoV-2 infection affects viral infection MESHD and host immune response. They support consideration of circadian rhythm in SARS-CoV-2 disease MESHD progression and we propose circadian rhythm as a novel target for managing viral progression. ImportanceThe implication of circadian rhythm (CR) in pathogenesis of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been recently anticipated. The time of day of infection is critical for illness progression as reported for influenza, respiratory syncytial and parainfluenza type 3 viruses. In this study, we wondered if SARS-CoV-2 infection and cytokine production by human monocytes, innate immune cells affected by Covid-19, were regulated by CR. Our results suggest that time day of SARS-CoV-2 infection affects viral infection and host immune response. They support consideration of circadian rhythm in SARS-CoV-2 disease progression and we propose circadian rhythm as a novel target for managing viral progression.

    Evaluating the effects of cardiometabolic exposures on circulating proteins which may contribute to SARS-CoV-2 severity

    Authors: Tom G Richardson; Si Fang; Ruth E Mitchell; Michael V Holmes; George Davey Smith; Dominik Schulz; Ulrich Mayr; Jochen Schneider; Christoph Spinner; Fabian Geisler; Roland M. Schmid; Tobias Lahmer; Wolfgang Huber; Xiushan Yin; Arsen Arakelyan; Denise Haslwanter; Rohit Jangra; Alev Celikgil; Duncan Kimmel; James H Lee; Margarette Mariano; Antonio Nakouzi; Jose Quiroz; Johanna Rivera; Wendy A Szymczak; Karen Tong; Jason Barnhill; Mattias NE Forsell; Clas Ahlm; Daniel T. Stein; Liise-anne Pirofski; Doctor Y Goldstein; Scott J. Garforth; Steven C. Almo; Johanna P. Daily; Michael B. Prystowsky; James D. Faix; Amy S. Fox; Louis M. Weiss; Jonathan R. Lai; Kartik Chandran

    doi:10.1101/2020.09.10.20191932 Date: 2020-09-11 Source: medRxiv

    Background: Developing insight into the pathogenesis of severe acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2) is of critical importance to overcome the global pandemic caused by coronavirus disease MESHD 2019 (covid-19). In this study, we have applied Mendelian randomization (MR) to systematically evaluate the effect of 10 cardiometabolic risk factors and genetic liability to lifetime smoking on 97 circulating host proteins postulated to either interact or contribute to the maladaptive host response of SARS-CoV-2. Methods: We applied the inverse variance weighted (IVW) approach and several robust MR methods in a two-sample setting to systemically estimate the genetically predicted effect of each risk factor in turn on levels of each circulating protein. Multivariable MR was conducted to simultaneously evaluate the effects of multiple risk factors on the same protein. We also applied MR using cis-regulatory variants at the genomic location responsible for encoding these proteins to estimate whether their circulating levels may influence SARS-CoV-2 severity. Findings: In total, we identified evidence supporting 105 effects between risk factors and circulating proteins which were robust to multiple testing corrections and sensitivity SERO analyses. For example, body mass index provided evidence of an effect on 23 circulating proteins with a variety of functions, such as inflammatory markers c-reactive protein (IVW Beta=0.34 per standard deviation change, 95% CI=0.26 to 0.41, P=2.19x10-16) and interleukin-1 receptor antagonist (IVW Beta=0.23, 95% CI=0.17 to 0.30, P=9.04x10-12). Further analyses using multivariable MR provided evidence that the effect of BMI on lowering immunoglobulin G, an antibody SERO class involved in protecting the body from infection MESHD, is substantially mediated by raised triglycerides levels (IVW Beta=-0.18, 95% CI=-0.25 to -0.12, P=2.32x10-08, proportion mediated=44.1%). The strongest evidence that any of the circulating proteins highlighted by our initial analysis influence SARS-CoV-2 severity was identified for soluble glycoprotein 130 (odds ratio=1.81, 95% CI=1.25 to 2.62, P=0.002), a signal transductor for interleukin-6 type cytokines which are involved in the bodys inflammatory response. However, based on current case samples for severe SARS-CoV-2 we were unable to replicate findings in independent samples. Interpretation: Our findings highlight several key proteins which are influenced by established exposures for disease. Future research to determine whether these circulating proteins mediate environmental effects onto risk of SARS-CoV-2 are warranted to help elucidate therapeutic strategies for covid-19 disease severity.

    Development, clinical translation, and utility of a COVID-19 antibody test SERO with qualitative and quantitative readouts

    Authors: Robert H. Bortz III; Catalina Florez; Ethan Laudermilch; Ariel S Wirchnianski; Gorka Lasso; Ryan J Malonis; George I Georgiev; Olivia Vergnolle; Natalia G Herrera; Nicholas C Morano; Sean T Campbell; Erika P. Orner; Amanda Mengotto; M Eugenia Dieterle; Jens Maximilian Fels; Denise Haslwanter; Rohit Jangra; Alev Celikgil; Duncan Kimmel; James H Lee; Margarette Mariano; Antonio Nakouzi; Jose Quiroz; Johanna Rivera; Wendy A Szymczak; Karen Tong; Jason Barnhill; Mattias NE Forsell; Clas Ahlm; Daniel T. Stein; Liise-anne Pirofski; Doctor Y Goldstein; Scott J. Garforth; Steven C. Almo; Johanna P. Daily; Michael B. Prystowsky; James D. Faix; Amy S. Fox; Louis M. Weiss; Jonathan R. Lai; Kartik Chandran

    doi:10.1101/2020.09.10.20192187 Date: 2020-09-11 Source: medRxiv

    The COVID-19 global pandemic caused by severe acute respiratory syndrome coronavirus-2 MESHD (SARS-CoV-2) continues to place an immense burden on societies and healthcare systems. A key component of COVID-19 control efforts is serologic testing SERO to determine the community prevalence SERO of SARS-CoV-2 exposure and quantify individual immune responses to prior infection MESHD or vaccination. Here, we describe a laboratory-developed antibody test SERO that uses readily available research-grade reagents to detect SARS-CoV-2 exposure in patient blood SERO samples with high sensitivity SERO and specificity. We further show that this test affords the estimation of viral spike-specific IgG titers from a single sample measurement, thereby providing a simple and scalable method to measure the strength of an individual's immune response. The accuracy, adaptability, and cost-effectiveness of this test makes it an excellent option for clinical deployment in the ongoing COVID-19 pandemic.

    Clinical course and management of 73 hospitalized moderate patients with COVID-19 outside Wuhan

    Authors: Xiaojuan Peng; Qi Qi Liu; Zhaolin Chen; Guiyan Wen; Qing Li; Yanfang Chen; Jie Xiong; Xinzhou Meng; Yuanjin Ding; Ying Shi; Shaohui Tang

    doi:10.21203/rs.3.rs-76135/v1 Date: 2020-09-11 Source: ResearchSquare

    Background: Moderate cases account for the majority in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection MESHD and can also progress to severe/critical condition. Here, we investigated the clinical course and management of hospitalized moderate SARS-CoV-2 patients.Methods: The medical records and follow-up data were analyzed from the SARS-CoV-2 patients outside Wuhan.Results: A total of 73 moderate patients (38 men, 35 women) were included, with median age TRANS of 47.0 (38.5-57.5) years. Among them, only one patient (1.4%) died using active treatment to improve symptoms. The median duration of the four main symptoms cough HP, fever HP fever MESHD, chest tightness HP chest tightness MESHD, and fatigue HP fatigue MESHD were about 1-2 weeks; the median duration of the positive nucleic acid test (NAT) results for SARS-CoV-2 was slightly more than 2 weeks; the median hospitalization time was almost four weeks in 72 moderate survivors. The duration of cough HP cough MESHD and fever HP fever MESHD was positively correlated with the duration of the positive NAT results. On admission, 50% had lymphopenia HP lymphopenia MESHD; less than 30% had abnormal blood SERO biochemistry findings involving hyperglycemia HP hyperglycemia MESHD, liver function and myocardial enzymes. At discharge, the laboratory indexes were substantially improved. Two weeks after discharge, 5.6% survivors experienced a recurrence of the positive NAT results. Conclusions: Moderate SARS-CoV-2 patients have a good prognosis by the active treatment. After discharge, it is necessary that moderate survivors undergo at least a 2-week collective medical observation in quarantine places, which can identify and treat a proportion of patients with re-positive NAT results and to prevent the spread of the potential sources of infection MESHD.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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