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Source: COVID-19 Genetics  Dec 13, 2020  3 years, 4 months, 4 days, 13 hours, 52 minutes ago

COVID-19 Genetics: University of Edinburgh Study Confirms That Genes Are Critical To New COVID-19 Treatments

COVID-19 Genetics: University of Edinburgh Study Confirms That Genes Are Critical To New COVID-19 Treatments
Source: COVID-19 Genetics  Dec 13, 2020  3 years, 4 months, 4 days, 13 hours, 52 minutes ago
COVID-19 Genetics: Researchers from the University of Edinburgh have identified potential treatments for COVID-19 after the discovery of five genes associated with the most severe form of the disease. The genes: IFNAR2, TYK2, OAS1, DPP9 and CCR2 partially explain why some individuals become desperately sick with COVID-19, while others are not affected.


 
According to the study team’s abstract, host-mediated lung inflammation is present and drives mortality in critical illness caused by COVID-19. Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development.
 
The study team reported the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study (GWAS) in 2244 critically ill COVID-19 patients from 208 UK intensive care units (ICUs). They identified and replicated novel genome-wide significant associations, on chr12q24.13 (rs10735079, p=1.65 ×× 10-8) in a gene cluster encoding antiviral restriction enzyme activators (OAS1, OAS2, OAS3), on chr19p13.2 (rs2109069, p=2.3 ×× 10-12) near the gene encoding tyrosine kinase 2 (TYK2), on chr19p13.3 (rs2109069, p=3.98 ×× 10-12) within the gene encoding dipeptidyl peptidase 9 (DPP9), and on chr21q22.1 (rs2236757, p=4.99 ×× 10-8) in the interferon receptor gene IFNAR2.
 
The team identified potential targets for repurposing of licensed medications: using Mendelian randomization they found evidence in support of a causal link from low expression of IFNAR2, and high expression of TYK2, to life-threatening disease; transcriptome-wide association in lung tissue revealed that high expression of the monocyte/macrophage chemotactic receptor CCR2 is associated with severe Covid-19.
 
The study results identify robust genetic signals relating to key host antiviral defense mechanisms, and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. Large-scale randomized clinical trials will be essential before any change to clinical practice.
 
The study findings were published in the peer-reviewed journal: Nature https://www.nature.com/articles/s41586-020-03065-y
 
The current trend is such that genetic evidence is second only to clinical trials as a way to tell which treatments will be effective in a disease. Existing drugs that target the actions of the genes reveal which drugs should be repurposed to treat COVID-19 in clinical trials, experts say.
 
The genes involved in two molecular processes ie antiviral immunity and lung inflammation were pinpointed.
 
The breakthrough discovery will help physicians understand how COVID-19 damages lungs at a molecular level.
 
The study team made the discovery by studying the DNA of 2,700 patients in 208 intensive care units (ICUs) in the UK.
 
The study team from the GenOMICC consortiuma global collaboration to study genetics in critical illness and c ompared the genetic information of COVID-19 patients in ICU with samples provided by healthy volunteers from other studies, such as UK Biobank, Generation Scotland and 100,000 Genomes.
 
The researchers found key differences in five genes of the ICU patients compared with samples provided by healthy volunteers. The genes IFNAR2, TYK2, OAS1, DPP9 and CCR2 can partially explain why some people become desperately sick with COVID-19, while others are not affected.
 
After having discovered the genes, the study team was then able to predict the effect of drug treatments on patients, because some genetic variants respond in a similar way to particular drugs.
 
For instance the team showed that a reduction in the activity of the TYK2 gene protects against COVID-19. A class of an