Breakthrough Findings on Why Only Certain COVID Patients Die
According to Health Secretary Rajesh Bhushan, 53 percent of those who died as a result of the Covid-19 viral infection were over 60 years old. In comparison, 35% of the coronavirus deaths occurred in the 45-60 year old age group, 10% in the 26-44 year old age group, and 1% in the 18-25 year old and under 17 year old age groups. Advanced age and underlying medical conditions are some of the reasons why certain patients with Covid-19 die. Scientists are trying to find are there any other reasons apart from these factors which make certain patients more susceptible to severe illness and death. When we can find an answer to this question, we may be able to find targeted therapies for Covid-19. The COVID human genetic initiative led a survey involving 200 research centers in 40 countries. Antibodies that disable interferons were found in 10% of approximately 1,000 COVID patients who experienced life-threatening pneumonia, according to results reported in Science. These interferons are key proteins of the immune systems. In 663 patients with mild or asymptomatic COVID Infections, these interferon autoantibodies were not identified. The study also revealed that only four out of the 1,227 healthy individuals had these autoantibodies. In another study, the same team found that 3.5 percent of chronically ill patients had mutations in genes that regulate interferons. Our body has 500 to 600 genes that code for interferons and researchers are likely to identify more mutations in interferons. Interferons are the first line of protection against viral pathogens, and they are in charge of activating virus-fighting genes. Invitro studies identified that interferons are suppressed by the virus in certain patients with Covid-19. When infected with the novel coronavirus, our body’s alarm system should ring and interferons need to be activated. If the activation fails, the viruses may multiply in larger numbers. Researchers speculate that these autoantibodies never caused problems until patients are infected with Covid-19. The Covid-19 per se or the triggered immune response may cause the problem. Autoantibodies against interferon are now being studied to see how they raise the risk of other viruses, such as influenza. Another surprising result was that autoantibodies were found in 94 percent of the patients in the sample. Autoantibodies against interferon were used in 12.5% of men and 2.6 percent of women with life-threatening COVID pneumonia. In addition, some genes implicated in the immune response to viruses have been discovered on the X-chromosome, according to a Yale University professor of immunology. X chromosomes are found in two copies in women. As a result, if one copy of the gene is faulty, the other copy will be able to shield them. As men have only one X-chromosome, when one copy of the gene is defective, there is no other copy to correct the issue. One of the women in the study who developed autoantibodies was born with only one X-chromosome, which is an unusual genetic disorder. Hormonal causes are involved. Estrogen hormone seems to have a protective effect and testosterone puts men at an increased risk of developing a severe disease in men. Though women may develop the less severe illness than men, they are more likely to experience long-term COVID symptoms that may last for a a few weeks to months.
Patients who obtained an inhaled form of interferon beta-1a were more than twice as likely than those who did not to survive and regain their normal activities, according to a pilot study of 98 patients. The analysis must be conducted in a broader number of patients to support the findings. Furthermore, since inhaled interferon is administered straight to the lungs, it seems to function easier. However, a study led by WHO found no benefit of these injected interferons and the findings need to be approached with caution.