May 19, 2024

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Science: Men’s death risk significant higher than women’s if COVID-19 infected

Science: Men’s death risk significant higher than women’s if COVID-19 infected


Science: Men’s death risk significant higher than women’s if COVID-19 infected. Because one chromosome is different, the risk of death in men with new coronavirus pneumonia is significantly higher than in women.


A comprehensive survey recently published in Science magazine pointed out that the risk of death in men with new coronavirus pneumonia is 1.7 times higher than that in women.


What caused the difference in death of different sexes? This involves various factors. For example, the prevalence of chronic diseases such as heart disease, diabetes, and obesity in men is significantly higher than that in women. These are high-risk factors that cause severe illness after infection. Some highly labor-intensive jobs are mostly men, which also increases the risk of infection and severe illness.


Takehiro Takahashi, professor of immunology at Yale University School of Medicine in the United States, pointed out that in addition to gender differences in underlying diseases and social roles, men’s own immune response systems are weaker than women.

Therefore, they are more likely to become severely ill when faced with a new coronavirus infection. There are many pathogens in nature that can produce different disease consequences for different people, but the immune response of men is often weaker, including hepatitis B virus, HIV, etc., and men are more susceptible than women.

At the same time, women’s immune response to vaccines is usually stronger than that of men. Of course, women’s stronger immune response also makes them more susceptible to autoimmune diseases than men.


What is the difference between the immune response of men and women? Takehiro explained that after the human immune system recognizes the virus replication signal in the body, it initiates two antiviral immune programs. The first is a cellular antiviral defense program mediated by interferon to limit the replication and spread of viruses; the second is to produce cytokines and chemokines to promote the activity of immune cells such as monocytes and neutrophils, Phagocytosis eliminates infected cells.


In the early stage of viral infection, the concentration of innate immune cytokines and chemokines in the plasma of male patients increases, while the concentration of plasma interferon in women is higher throughout the course of the disease. A research report on critically ill patients found that some patients have autoantibodies that inhibit the activity of interferon. 94% of these patients are elderly men. Older female patients have highly activated T cells in the early stage of infection, while men’s T cell activation ability decreases significantly with age. Males with poor T cell activation tend to become severely ill after infection, while females are not affected.


Takehiro analyzed that, at the root, the difference between male and female comes from a pair of sex chromosomes: female is XX, male is XY, and a large number of important immune-related genes are encoded on the X chromosome, such as those that can produce a strong interferon response. Toll-like receptor 7, etc., are all on the X chromosome. Therefore, when women are infected by pathogens such as the new coronavirus, the interferon response is stronger and the protective effect is better.


Gender also determines the difference in the degree of aging of the immune system. The male immune system accelerates aging from 62 to 64 years old, and the number of immune B cells declines at the age of 65. At this time, the expression of innate pro-inflammatory genes increases, and the expression of genes related to adaptive immunity decreases. Therefore, elderly men are prone to excessive inflammation and poor adaptive immune responses. In comparison, the accelerated aging of the immune system of women is 5 to 6 years later than that of men. This is also related to the rule that women in many countries live longer than men by about 5 years.


Estrogen also has a protective effect against the new coronavirus. Estrogen can affect the activity of angiotensin converting enzyme (ACE2), which is an important channel for viruses to infect cells. The estradiol in estrogen has proven to inhibit monocytes and macrophages from producing excessive innate inflammatory cytokines, reducing the risk of excessive immune response after infection. Menopause is one of the independent factors leading to female infection risk, and male prostate cancer patients have a reduced risk of viral infection after receiving endocrine therapy, which also proves the role of estrogen.


Gender affects the new coronavirus pneumonia vaccine response and the risk of secondary infection. Some studies on plasma antibodies in the recovery period have found that elderly men tend to produce higher antibody titers after recovery from hospitalization. This may be related to the severity of their illness. The increase in viral load can drive more B cells to activate to produce antibodies; on the other hand, a higher number of antibodies means that the immune compensatory response is excessive, and the quality of antibodies in elderly men is poor. Can not effectively neutralize the virus.


Takehiro pointed out in the summary that due to the significant differences in the immune response of different genders to infection, we should classify the new coronavirus reports according to gender. Through such research methods, we can further clarify the pathogenesis of the disease, gain an in-depth understanding of the disease, and formulate better treatment and prevention strategies. Not only the new coronavirus, but also other infectious diseases and vaccine research should include gender as one of the most important classification basis.




(source:internet, reference only)

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