BEIJING, May 6 (Xinhua) — Individual differences in genetic composition may explain human susceptibility to the new coronavirus and the severity of the disease, according tomedia reports. Since the outbreak of the new coronary virus a few months ago, scientists have been trying to explore ways to analyze the virus’s different manifestations, ranging from asymptomatic cases to severe cases involving acute respiratory distress syndrome, which can lead to death, and what causes individual differences in patients with the new coronavirus. Does this have to do with human genes?
Scientists have been questioning coronavirus for more than a decade, and back in 2003, when the SARS virus exploded globally, Ralph Baric of the University of North Carolina at Chapel Hill and colleagues found a gene that, if mutated and suppressed, made experimental mice susceptible to SARS. The gene, called TICAM2, encodes proteins to activate a series of receptors called bell receptors (TLRs), which are associated with the innate immune system and are the first line of defense against pathogens.
Researchers are once again interested in TLRs receptors for the new coronavirus that is currently ravaging the world, which may help explain the high number of men suffering from serious infections.
On April 23rd a survey published in France showed that 73% of all patients with new coronaviruses in the intensive care units of French hospitals may be related to differences in their behavioural characteristics and hormones, but genes may be a mixed factor, unlike men, women have two X chromosomes and therefore carry twice the TLRs gene, an important viral activity indicator that helps boost immunity.
Blood-type genetics can identify whether people are susceptible to the virus, and the researchers found that A blood type appears to be associated with a higher risk of infection, while The o-blood type has the greatest protective effect, for which the exact reason is not clear.
The SARS virus, which broke out in 2003, offers lessons from the presence of two different sugar molecules on the surface of red blood cells, each of which is produced by an enzyme in two forms: type A and B. The third gene variant encodes an inactive enzyme, type O, and the person with the variant synostic adenoids is the AB blood type.
Each sugar molecule (type A or B) can be used as an antigen, which can trigger the production of antibodies against the antigens it lacks, which is why people must be very careful when they are blood transfusions. In the ABO blood type system, the O blood type population has the most body antibodies, it has both A and B antibodies, while the AB blood type population does not have these two antibodies.
In 2008, Jacques Le Pendu, a researcher at the University of Nantes in France, and colleagues investigated an in vitro model sample of the SARS virus, which showed that the binding of viral protein S to cell ACE2 (type 2 vascular tensor-transformation enzyme) receptors was an essential process of viral infection, which was inhibited by type A antibodies, but their data on type B antibodies were still scarce.
In the blood pressure control process, a close relative of ACE2 is “type 1 vascular tensor transformation enzyme (ACE1),” the ACE1 D gene is one of several gene mutations of the conversion enzyme, and eventually the receptors allowed to infect SARS virus in the cell are significantly reduced.
The emergence of the ACE1 D gene is related to the countries and regions in which people live, especially in Europe, and scientists believe that the geographical distribution of the population of the variant is related to the spread of the new coronavirus, does this index reflect the extent to which the new coronavirus is spreading globally? ‘This is true, ‘ says Marc De Buyzere, a researcher at the University of Ghent in Belgium. ‘My colleagues and I believe that the ACE1 D gene population is closely related to the susceptibility of the new coronavirus.’
Based on data from 25 countries (including Portugal, Estonia, Turkey, Finland and other countries), the researchers found that 38 percent of changes in the prevalence of neo-coronaviruses could be explained by the frequency of the ACE1 D gene, and that mortality statistics showed a similar correlation. They say the ACE1 gene is less frequent in Asian countries where the virus is severely infected with the new coronavirus.
More of the genetic component of the new coronavirus susceptibility may be related to the genetic coding of human leukocyte antigens (HLAs), a group of proteins that prevent the body’s immune system from being attacked by viruses, and form a “major tissue-compatible complex (MHC)”, which marks “self-composition” and distinguishes it from “non-self-components.” Now, Reid Thompson, a researcher at Oregon Health Sciences University, and colleagues have found a close link between specific HLA genes and the level of neo-coronavirus infection.
Carrying a mutant gene called HLA-B?46:01 is more susceptible to SARS, thompson said, as has previously been shown to be a new coronavirus susceptibility, compared to the HLA-B-15:03 mutation that may provide some protection. By identifying someone’s HLA genetic characteristics, testing can be done quickly and cheaply, which may help better predict the extent of infection, and even help determine who will be better vaccinated.