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Hidden Mutations Could Spell The Difference Between A Mild Flu And A Fatal One

We've blamed flu deaths on socioeconomic factors and pre-existing conditions. New research suggests our fate could lie hidden deep within the infected cell.

10/23/2017 15:51 EDT | Updated 10/23/2017 15:51 EDT

When flu strikes, most people feel horrible, but they usually don't fear for their lives. That all changed in 2009 when the pandemic "swine flu" virus — officially known as H1N1pdm — came around. During those months, deaths were common in some parts of the world. But the toll on life wasn't universal, as some countries suffered far worse than others.

At first, this phenomenon appeared to be due to socioeconomic factors. Poorer countries seemed to suffer the most due to a lack of proper medical treatment. In higher-income countries, like Canada, those who had pre-existing conditions such as diabetes, cardiac disease and compromised immunity were more likely to face a life-or-death situation. The explanations made sense.

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For a group of Spanish researchers, however, this explanation wasn't sufficient. They figured the nature of the virus itself might play a role. In 2013, they examined the H1N1pdm viruses isolated from a fatal case and a mild case. They hoped to identify differences in the way the virus lived inside cells and if there were any differences in the way the host — in this case, mice — responded.

The experiments revealed the two isolated viruses were quite different from one another even though they were both the same H1N1pdm species. The fatal flu led to a rather dramatic immune response known as a cytokine storm. The individual suffered a microscopic fog of war that spread through the body and became life-threatening. The mild flu, on the other hand, led to no such problems. The immune system acted normally and was able to clear the infection.

The results seemed to suggest the virus may have a greater role in determining the extent of infection. Yet, the information didn't reveal what that might have been. The team figured they needed to look even closer at the virus — inside the cell — to get an answer.

The results imply our fate could lie in a few small changes hidden deep within the infected cell.

Last week, they finally found what could be the reason. As they expected, the secret had to do with the inner workings of the virus. While fascinating, the results imply our fate could lie in a few small changes hidden deep within the infected cell.

When influenza enters a cell, its one job is to make more copies of itself. This process, known as replication, has been studied for decades. It's best described as a hijacking in which the cell can no longer perform its usual functions and instead serves to make hundreds of new viruses. These viruses then escape from the cell in search of another victim.

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But the process isn't perfect. For every good virus, there are thousands of copies of the genetic material — known as the genome — that never make it. These are known as defective viral genomes, or DVGs. From a health perspective, these DVGs are useful to us in the fight against the virus as they inadvertently signal the immune system that something is going on. The result is a quicker response to the invasion and possibly milder symptoms.

These DVGs were the focus of the Spanish researchers' study. They wanted to find out whether the fatal and mild flus showed a difference in the number of DVGs. They tested the viruses both in the laboratory as well in mice. If they were right, the fatal strain would make fewer DVGs than mild strain.

It all came down to a few particular mutations.

When the results came back, they were not disappointed. The fatal strain was doing a better job of making proper viruses while the mild strain was producing a high number of DVGs. The team even managed to find out how this was happening. It all came down to a few particular mutations. When one or more of these changes happened, there was a tremendous improvement in the virus manufacturing process.

The results of the study are somewhat disheartening as we cannot figure out in real time whether these mutations exist. Figuring out how to quickly detect these changes may help to predict whether a flu season may be relatively normal or end up being troublesome. Until then, we have to rely on keeping the virus out of our bodies.

Thankfully, we know how to minimize the chances for infection. The regular use of handwashing and hand sanitizers, as well as proper disinfection of surfaces, will help keep us safe. Then there is the most useful option in the form of vaccination. By being protected against the virus, you won't have to worry about whether the infection could cost you a few days — or possibly your life.

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