We still do not understand COVID-19, but scientists have gone a step further in finding out why some patients reach critical stages of the disease. A new study of thousands of COVID-19 patients revealed eight genetic sequences that are more common among individuals who develop life-threatening events.
This finding not only helps to develop new drugs to help in the treatment of the virus, but also points to current drugs that can help recover critically ill patients.
“We have discovered new and more reliable genetic links to complex diseases in COVID-19,” explains a new study by a team of international researchers led by the University of Edinburgh in the UK.
“Some of these associations directly lead to potential therapeutic approaches to enhance interferon signals, inhibit monocyte activation and infiltration into the lungs, or specifically target inflammatory pathways.”
The researchers conducted their research on 2,244 malignant COVID-19 patients from 208 intensive care units in the UK. Their DNA was subjected to a genetic scale association study (GWAS), in which the genetic variants of individuals are analyzed to determine whether they are related to a particular trait.
Control genes that are compatible with descent were selected from UK Biopank, an anonymous genetic database on a population scale. For each COVID-19 patient, five controls were selected, which did not appear to have a positive COVID-19 test.
GWAS showed that eight gene sequences were the most common in COVID-19 patients, which was verified using two independent demographic studies. Five scenarios were reflected in the COVID-19 host genetic initiative and in the meta-analysis of COVID-19 patients of 23andMe Inc.’s broad respiratory phenotype.
This may not be particularly effective on an individual level, as most humans do not sequence their genes. However, what genes do can be used to develop therapy.
The researchers found that the sequences were related to genes involved in inflammatory processes and the body’s response to invading viruses.
“For example, the TYK2 gene is associated with inflammatory responses that are known to cause ‘cytokine storms’, leading to the death of younger patients. [this] Condition, ”said David Strain, senior medical lecturer at the University of Exeter and the British Medical Association, who is not involved in the research.
“The reason this is of interest is that there are treatments to prevent this (JAK receptor) receptor, so they may be [a] Therapeutic preference goes forward (especially for individuals experiencing cytokine storms below the priority list for vaccines). “
A link between severe COVID-19 and a genetic predisposition to obesity was also of interest. This means that lifestyle changes do not have a major impact on COVID-19 effects.
There is at least one significant limitation in the study, Strain notes: The controls have not been tested in favor of COVID-19.
“Ideally, in order to differentiate those with severe disease, all controls would have been exposed to the corona virus, and we would compare those who tested positive, but only those who were hospitalized with mild disease,” he said.
Overall, however, the team’s findings suggest that there are two biological mechanisms behind the significant disease in COVID-19. In the early stages, the body’s innate immune response to a viral infection; And in the last stages, inflammatory processes in the body.
Because there are already drugs that can target these pathways – TYK2, for example, are targeted by the rheumatoid drug paracetamol – clinical trials can be carried out quickly to test the findings.
Research has been published Natural.