Why infections make us age faster – 01/31/2024 – Balance

From every infection that our immune system defends us against, we not only emerge tired, but also a little older.

The latest research suggests that biological age may be much higher than normal in people who have had multiple viral infections or who suffer from a chronic infection.

In these cases, it is not uncommon for a person with a chronological age — that of the identity document — of 40 to have an immune system similar to that of a 60-year-old individual. And this can profoundly impact the quality of life and functioning of defense cells.

But how does this happen? How is a virus capable of causing a person to age?

To understand this phenomenon, we must remember that the genetic information we inherit from our parents is stored in chromosomes, that is, in super-packaged DNA structures shaped like an X.

And, to maintain this DNA structure stable, chromosomes need to have structures at the ends that function as “protective helmets”. They are called telomeres.

Division implies wear

Of Greek origin, the word telomere literally means “end part”. The function of this structure is to prevent chromosomes from breaking or being damaged, as they are weaker at the ends.

It’s as if chromosomes were made of wool: without these protective helmets, they would be at risk of wearing out and simply falling apart.

The body’s cells are not the same when we are born and when we die: throughout life, they are renewed through successive divisions in which, from a single cell, two identical daughter cells are formed.

Each cell division causes a small amount of wear and tear on the telomeres, which become shorter and shorter. This is something we know in scientific jargon as telomere shortening.

After a certain number of divisions, these structures become so small that they can no longer fulfill their protective function. As a result, the chromosome begins to wear out and lose its original formation.

When this occurs, cells are unable to divide and perform functions as expected.

In a way, telomeres act like cellular clocks. They are able to measure how many times a cell can divide. And it is normal for older people to have more worn-out telomeres than younger people.

However, age is not the only process behind telomere shortening. This also occurs due to other factors, such as ethnicity, gender, stress, diet and exposure to certain diseases.

The effects of infections

When the immune system comes into contact with a harmful microorganism, a process of division and massive expansion of defense cells occurs, until they form a population large enough to destroy the invader.

This means that each infectious process gives rise to a cycle of massive immune cell divisions.

The consequence of this is telomere wear and an increase in the probability of entering what is known as immunosenescence earlier, that is, a state in which the immune system is aged.

The more infections we face throughout our lives, the more the telomeres of the cells that defend us shorten. And this, in turn, ages the immune system. Experts speak of “virus-induced senescence”.

Studies with patients infected with viruses such as HIV, Epstein-Barr (which causes mononucleosis) and hepatitis C, among others, have demonstrated a shortening of the telomeres of immune system cells.

Furthermore, studies have recently shown that patients with severe Covid-19 suffered telomere shortening.

Therefore, as we mentioned at the beginning of the article, biological age can be much higher than chronological age in people who have suffered multiple infections or who face a chronic infection.

Immune aging

As telomeres shorten and the immune system ages, cells lose the ability to defend us from infections. And this leads to a greater risk of suffering from infectious diseases.

This is the reason why the elderly respond worse to infections and — what is more worrying — also to vaccines.

For a vaccine to be effective, a properly functioning immune system is required.

There is also evidence that the shortening of telomeres prevents the regeneration of damaged tissues after infections through cell division, causing a significant proportion of patients to have sequelae or a greater risk of developing other conditions.

More infections and illnesses

The consequences of immunological aging are multiple.

On the one hand, the phenomenon has been related to a greater susceptibility to respiratory and urinary infections, infectious endocarditis (infection of the membrane that lines the heart chambers) and sepsis (presence of bacteria in the blood), as well as cancer, Alzheimer’s and autoimmune diseases. .

Autoimmune diseases are conditions in which the immune system attacks the body’s own cells: it seems logical to think that a defective immune system is more likely to “make a mistake” and attack healthy units.

There is no doubt that infections cause accelerated aging of the immune system, which leads to a greater predisposition to suffer from both infectious diseases and other pathologies.

This relationship between infections and aging, through telomere wear, requires further research to try to anticipate and design strategies capable of alleviating this wear.

*Raquel Behar Lagares, Amanda Fernández Rodríguez and María Angeles Jiménez Sousa are researchers at the National Center for Microbiology at the Carlos III Health Institute, in Spain.

**This article was originally published on The Conversation and republished under a Creative Commons license. Click here to see the original (in Spanish).