Your immunity is related to the year of birth.

Some types of viruses have a high ability to mutate and can infect people repeatedly.

Sometimes, the secondary infection may be more serious than the primary infection.

This problem arises precisely because there is an unsolved "loophole" in the powerful immune system.

Every winter and spring, influenza arrives as expected, and they seem to be lurking around us, waiting for the opportunity to pounce on the crowd again and again.

Among the influenza viruses, there is one kind of virus-influenza A virus (influenza A viruses), which is feared because of its infectivity and pathogenicity.

It has caused several influenza pandemics and caused great harm to human beings.

Some strains of these viruses persist for a long time in animals such as wild birds, poultry and pigs.

Some of these strains, when mutated, can cause host disease or infect humans through cross-species transmission, leading to larger outbreaks, such as the H1N1 virus that caused the 1918 pandemic (the original host was pigs).

From the Spring Festival in 2009 to August of the following year, a new strain of H1N1 virus made a comeback, causing another influenza pandemic.

Which flu is more serious?

H and N on influenza A virus, including H1N1 virus, refer to two antigens, hemagglutinin and neuraminidase, respectively.

They are two easily mutated glycoproteins.

According to the type of hemagglutinin, influenza A viruses are divided into type A (H1, H2 and H5) and type B (H3, H7).

H5N1 is a highly pathogenic avian influenza, which is highly contagious and lethal in birds. It was first found to infect humans in 1997. The mortality rate of humans infected with this virus is about 60%.

The rate of severe illness and mortality caused by H7N9 was slightly higher than that of SARS in 2003.

These two viruses cause hundreds of severe symptoms or deaths each year.

Generally speaking, when the human body is first infected by a pathogen and cleared of it, the body will form an immune memory.

If you encounter the virus at a later stage, memory cells are activated and they can react quickly to speed up the elimination of pathogens.

In this study, some people were born before 1968 and experienced outbreaks of influenza A viruses such as H1N1 and H2N2, and then influenza B viruses such as H3N2.

In theory, they should have good immunity to influenza An and B influenza viruses, but the fact is that they have low immunity to influenza B viruses and are more likely to develop severe symptoms due to H7N9 infection.

In 2009, the H1N1 flu outbreak, this time the virus is a new H1N1 variant.

Scientists at that time noticed a phenomenon that when infected people came into contact with a new variant of influenza virus, they were more likely to produce a widespread antibody that could bind to common sites on both new and old virus antigens, but few antibodies bound to new sites on new virus antigens.

This often leads to a problem, that is, the body is constantly producing new antibodies, but cannot completely kill the new virus.

In the 2016 study, scientists speculated that a person's immunity to the flu virus in his lifetime is related to his year of birth (because different flu strains are prevalent at different times).

In other words, the first influenza virus that comes into contact with in life will affect that person's immunity to the virus in the future.

The "lazy" immune system.

As early as 1960, Thomas Francis Jr., the first American scientist to isolate the influenza virus, described this phenomenon, which he called immunogenic sin (original antigenic sin).

The specific explanation is that the body's immune system will be subject to the immune response caused by the antigen of the first contact. When a new strain formed by the mutation of the virus (or bacteria) appears later, the immune system will still use the initial immune response to fight the new virus, but will not produce new antibodies against the new strain, resulting in a decrease in immune ability.

This phenomenon is related to the immune memory of the human body.

During the first infection, the body produces long-lived memory B cells.

When they encounter the same infection later, these memory cells can quickly identify the pathogen and activate the immune response.

This process is faster than re-identifying the virus, giving the immune system an advantage in time and reducing the degree of damage to the body.

However, when there are some genetic mutations in the antigens of the second invaded virus, the phenomenon of immunogenic sin may occur.

In other words, the antibodies produced by B cells are still directed against the first virus, and the affinity with the second infected virus will decrease, resulting in reduced immune response efficiency and repeated infection.

Some studies have found that the disease has an obvious epidemiological feature: it is easy to occur in people who have been infected once-usually the virus subtype of the second infection is not the same as that of the first, and patients are more likely to develop more severe symptoms. including dengue haemorrhagic fever and dengue shock.

This is not optimistic for infected people, and scientists generally believe that a hypothesis can explain this phenomenon-increased antibody dependence (Antibody-dependent enhancement).

After binding to the virus, some antiviral antibodies can be swallowed by macrophages.

But if the antibody is not specifically targeted at the new virus, its affinity with the latter will not be strong enough, and the virus will fall off from the antibody.

Dengue viruses, in particular, can infect macrophages themselves, which is equivalent to antibodies that help them spread.

In addition, some researchers believe that dengue haemorrhagic fever is also related to the immunogenicity of Cytotoxic T lymphocyte,CTL (usually CD8+ T cells).

These T cells are the main killer T cells in the human body and can bind to almost any cell invaded by pathogens in the human body.

After identifying cells, they can release some cytokines, causing infected cells to die in a certain way.

In the late 20th century, scientists conducted an experiment in which mice were first infected with a primitive meningitis virus, LCMV, CD8+ in mice.