Scientists continue to look for reasons why coronavirus is strangely picky. Under comparable risk and human health conditions, some are ‘unnoticed’ and others are ‘sent’ for resuscitation.
Genes (and even ethnicity) as well as the history of children’s diseases are able to give an answer, according to the information gathered by Rus.LSM.lv.
Decent age and serious chronic illness (diabetes, cardiovascular, respiratory and oncological diseases) increase the risk of Covid-19 being severe and fatal. However, this does not eliminate the risk to the young and healthy, according to the World Health Organization at the end of the second year of the pandemic, “anyone at any age can become infected with coronavirus, become seriously ill and die from Covid-19.”
Moreover, in these two years, some people in various countries have not only become ill – even without symptoms – but have not been infected at all, while at risk of becoming infected. Scientists are studying the protective mechanisms of these people’s immune systems, hoping it will help find new ways to fight Covid-19.
During the first outbreak of the pandemic, researchers at University College London observed a group of doctors and nurses who were at high risk of becoming infected every day in hospitals full of Covid-19 patients.
The researchers concluded that about a tenth of these doctors, who had been guaranteed to be infected, did not show any symptoms of the disease. The test results were negative.
Their immune systems were somehow able to repel the coronavirus at the earliest stage of infection, before it could multiply. A so-called abortion infection occurred when a broken pathogen simply does not survive in the “host”.
There were no antibodies in the blood that developed when infected with the Covid-19 virus. However, there were T-cells in the immune system that recognize and kill the cells affected by the virus and provide long-term protection, including without the help of antibodies.
Probably because they are more likely to be exposed to infectious pathogens at work, their immune systems are well trained. However, the question remains as to why this did not happen to the majority of their coronavirus-infected colleagues who fell ill and died.
Another hypothesis explains the resistance of some people to the new coronavirus with a so-called immune imprint. Similarly, the immune response to Covid-19 may be mediated by memory of previous infections with SARS-Cov-2 relatives, the common cold coronavirus. However, it is not yet clear whether a person’s immune memory for their first infection with coronavirus in childhood provides additional protection or actually delays the immune response.
At the same time, researchers at the University of Oxford have said they have found a gene whose presence indicates a double risk of lung damage or that Covid-19 could cause death. A study published in early November said a “dangerous” version of the LZTFL1 gene was interfering with the protective mechanism of the epithelium that spreads through the walls of the alveoli of the lungs.
It was also found that the prevalence of this gene was not ethnically even, with around 60% of people of South Asian descent found in the study, but only 15% of people of European descent.
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