|drug3766||blood sampling for biobank Wiki||0.71|
|drug3779||carotid-femoral pulse-wave velocity Wiki||0.71|
There are 2 clinical trials
Background: There is a current worldwide outbreak of the novel coronavirus Covid-19 which originated from Wuhan in China and has now spread to 6 continents including 210 countries. There is still a lack of any report about severe acute respiratory syndromes (SARS-CoV-2) genetic polymorphisms which are associated with the susceptibility to infection. In addition, gene polymorphisms of MBL (mannose-binding lectin) associated with antigen presentation are related to the risk of SARS-CoV infection. Aim: To investigate the association of different genetic markers of different mechanisms of viral pathogenesis with the outcome of COVID-19. Methods: The study will include one hundred patients diagnosed as COVID-19. Biological blood samples will be taken for routine diagnostic analysis, routine molecular testing using Real-time polymerase chain reaction (PCR), Allelic discrimination and genotyping analysis. Outcome: Different genetic markers could play a role in the outcome and prognosis of COVID-19 viral infection.
Description: To assess genetic mutation via detection of genetic polymorphisms of ACE2 in patients and control to detect what alleles will be associated with the susceptibility to COVID-19 and what alleles will be associated with clearance or protection from infections. using allelic discrimination SSCP (i.e Real-time PCR and genetic sequencer).Measure: for the patients Time: 2 years
The main objective of this part of the project is to identify the germline genetic factors which discriminate the benign and severe forms of SARS-CoV2 (CoVID-19) infection in the context of the ongoing SARS-CoV2 (HCOVID-19) epidemic. The scientific arguments of the project are described in APPENDIX. We hypothesize that pathogenic variants in genes coding for crucial factors involved in the HOST PATHOGEN interaction could explain the susceptibility of some patients to severe disease, even in the absence of comorbidities. The challenge is to identify those of the genetic factors who may be related respiratory distress and potentially further death. Based on our previous experience in sarcoidosis, a multifactorial disease predisposing to opportunistic infections, we will focus particularly the regulation of apoptosis and autophagy, immune response to viral infection, and endoplasmic reticulum stress response (ER STRESS) which is closely linked to apoptosis. Genetic defects in such pathways may decrease the clearance of viral particles and induces the progressive invasion by SARS-CoV2 and destruction of lung parenchyma. Our strategy will be similar to that described in our previous studies on sarcoidosis, recently published. We will combine a comparative genotype analysis by WHOLE EXOME SEQUENCING (WES) of benign and severe forms of SARS-CoV2 infection through clinical subgroups defined by the infectious diseases experts and a bioinformatics analysis of the functional networks identified by the panel of genes sharing pathogenic variants and discriminating the severe forms of the diseases. WES data will be carefully analyzed and related to all the intracellular physiological process and also the functional pathways involved in host-pathogen interaction: viral targets on the cell surface and downstream signaling, viral genomic RNA replication and translation, production and release of new viral particles. Finally, our main objectives are the definition of a gene panel more specifically related to severe forms of infection and the characterization of defective pathways involved in pejorative forms of SARS-COv2 disease in order to identify putative therapeutic targets.
Description: Number of genes affected by pathogenic variants in the SEVERE GROUP and for which no mutations have been observed in the CONTROL group For each gene sharing variants in the SEVERE GROUP and not in CONTROLS, the protein encoded by this gene will be identified and his function analyzed in the frame of various protein network software. The frequency of each mutation, so called the minor allele frequency will be evaluated in order to highlight only those which are rare (MAF < 0,01) in the normal population and thus suggesting a putative pathogenic role in the response to SARS-CoV2 infection.Measure: Primary criteria of data evaluation Time: through study completion, average 6 months
Data processed on January 01, 2021.
An HTML report was created for each of the unique drugs, MeSH, and HPO terms associated with COVID-19 clinical trials. Each report contains a list of either the drug, the MeSH terms, or the HPO terms. All of the terms in a category are displayed on the left-hand side of the report to enable easy navigation, and the reports contain a list of correlated drugs, MeSH, and HPO terms. Further, all reports contain the details of the clinical trials in which the term is referenced. Every clinical trial report shows the mapped HPO and MeSH terms, which are also hyperlinked. Related HPO terms, with their associated genes, protein mutations, and SNPs are also referenced in the report.Drug Reports MeSH Reports HPO Reports