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The COVID-19 pandemic has caused considerable morbidity and mortality and has killed more than one million people to date. The clinical manifestations of disease caused by the virus are known to vary widely in severity, from mild or no symptoms to rapid progression to respiratory failure. Now scientists have discovered the five genes that a person may have that indicate the severity of a COVID-19 infection.
A major study of 2,700 COVID-19 patients from 208 ICU wards gathered DNA and was able to find the genes that make a person more likely to die from the new coronavirus or be admitted to intensive care.
The researchers found five genes that increase a person’s severity against the virus and hope that by identifying them they can become drug targets.
The landmark study from the University of Edinburgh gathered DNA from 208 intensive care units in the UK for analysis.
The genetic information of these 2,700 patients was then compared to 100,000 anonymous Britons with five genes emerging as precursors to a serious COVID infection.
READ MORE: Coronavirus Symptoms: Scientists Warn of Fourth Key Warning Sign of COVID-19
The five genes found were:
TYK2
This gene encodes a member of the tyrosine kinase and, more specifically, the Janus kinase (JAK) protein families.
The TYK2 gene creates an enzyme that can cause inflammation.
This protein associates with the cytoplasmic domain of type I and type II cytokine receptors and promulgates cytokine signals by phosphorylation of receptor subunits.
It is also a component of the type I and type III interferon signaling pathways. As such, it can play a role in antiviral immunity.
Cytokines play a critical role in immunity and inflammation by regulating the survival, proliferation, differentiation, and function of immune cells, as well as cells from other organ systems.
CCR2
It can target drugs that are in trials but not widely used for psoriasis.
The evidence for this gene is not as strong as that for other genes in the study, but Dr. Baillie says it remains “compelling.”
OAS1
It is a gene that initiates a signal that activates an enzyme that breaks down virus-derived RNA.
Several other coronaviruses have a way of preventing this mechanism. There is no evidence yet for SARS-CoV-2, but it could be a specific feature that does.
It can target a class of drugs called phosphodiesterase 12 inhibitors.
These are not currently in clinical trials, but would theoretically enhance the antiviral effect of this system.
IFNAR2
This is a critical part of signaling that is responsible for the host’s antiviral response.
Signposting on this road is important in the possibility of getting sick.
Relevant to fight the virus directly, just like OAS1. This is most important early in the illness, as later on, virus levels drop and the problem comes from the body’s immune system attacking itself.
DPP9
It’s known to play several roles in inflammation, but researchers don’t yet know exactly where it fits in the progression of Covid-19 disease.
Therefore, they cannot make a direct therapeutic prediction.
It is associated with pulmonary fibrosis and could be associated with ‘prolonged covid’.
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