Spanish Flu: Why the epidemic that killed millions of people was so deadly? | Science and health

There was the outbreak of 1957 (the saying flu Asian) and the Hong Kong flu, in 1968. Forty years later, in 2009, it was the turn of the swine flu.

Each of these pandemics had similar origins, derived, one way or another, from an animal virus developed and pbaded on to humans. However, the major difference between them was the number of deaths.

It is estimated that the 1918 Spanish flu pandemic claimed the lives of 40 million people, compared to 2 million in Asia and Hong Kong, and 600,000 in swine flu, with a mortality rate of less than 1%.

The human cost of the 1918 pandemic was so high that many doctors continue to describe it as "the greatest medical holocaust in history". But what made her so deadly? And could this knowledge help us prepare for a similar pandemic in the future?

Understanding these pandemics would be impossible without the enormous advances in medicine during the twentieth century: the doctors of 1918 had just discovered the existence of the virus.

"And they did not know that a virus was causing these diseases," says Wendy Barclay of Imperial College London University, one of the largest in the UK -United. There were also no antiviral drugs or vaccines that could now help stop its spread and speed up the patient's recovery.

Many deaths from influenza are also caused by secondary bacterial infections that occur in the weakened patient, leading to complications such as pneumonia. Antibiotics such as penicillin – discovered in 1928 – now allow doctors to reduce this risk, but in 1918, this treatment no longer existed.

"Our health infrastructure and diagnostic and treatment tools are much more advanced today," says Jessica Belser, who works for the influenza service at the US Center for Disease Control and Prevention (CDC). .

In addition to the lack of basic medical tools in 1918, these deaths would also have been a direct result of the deplorable living conditions experienced at this tragic moment in the history of mankind. Trenches became an infection-prone environment for soldiers of the First World War.

"The virus appeared when populations, which previously had very little contact, were on the battlefield," said Patrick Saunders-Hastings of Carleton University in Ottawa, Canada. Canada. "And, in many cases, they were malnourished and were recovering from other wounds." Vitamin B deficiency, in particular, has increased mortality rates in subsequent pandemics, he said.

Even those who did not fight during the war lived in closed and populated environments, which eventually potentiated exposure to the virus. This not only accelerated the transmission, increasing the risk of infection, but also worsened the symptoms.

"We know that the higher the viral load, the more you get sick, because the virus is able to overload the immune system and stay more powerful in your body," says Barclay.

"We also know that the improvement of sanitation and hygiene conditions badociated with industrialization and the widespread reduction of poverty have considerably contributed to the reduction of mortality. by infectious diseases in the 20th century, "said Kyra Grantz of the University of Florida.

In badyzing documents filed in Chicago during the 1918 pandemic, Grantz showed that factors such as population density and unemployment directly affected the chances of contracting the disease.

It is interesting to note that the data also seem to show a close link between mortality risk and illiteracy rates in different parts of the city.

Indeed, illiteracy is an indicator of poverty. But it is possible that the lack of formal education of a person has also played a direct role in the progression of the disease.

"Public health officials have made considerable efforts to end the epidemic in Chicago, including around 40 throughout the city, school closures and the ban on public health. social agglomerations, "said Grantz. "But these measures are only effective if people understand why they are caught and adhere to them"

Despite these factors, many scientists believe that the virus itself was also particularly violent, even though it took more than a century. to understand exactly why.

At the time when the techniques of capture, storage, cultivation and badysis of viruses had been invented, the original strain had already disappeared. But recent advances in genomic technology have allowed scientists to resuscitate an active virus from inert historical samples. They then used it to infect laboratory animals, such as monkeys, and study their effects.

In addition to replicating very rapidly, the 1918 strain seems to trigger a particularly intense immune system response, including the rapid release of white blood cells and inflammatory molecules.

Although a strong immune response can help us fight the infection, an excessive reaction of this type can overwhelm the body, resulting in severe inflammation and fluid buildup in the lungs that can increase the risk of secondary infections.

This "immune storm" can help explain why young, healthy adults – who usually heal from a faster flu – have been the most affected, as their defense systems are more powerful.

But to understand why the 1918 strain would have this effect, we must go back to its origins.

It is thought that the 1918 flu is from a strain that normally infects birds – through mutations that have allowed it to infect the upper respiratory tract. This made it more easily transmitted in the air – by coughing and sneezing.

This aspect is important for two reasons. Without prior exposure to the virus, the body's immune system would not have been able to produce an effective response.

The fact that the virus itself is not yet fully adapted to life in the human body is just as important. Contrary to what many people think, it is not in the interest of a virus to kill its host.

"It is not good that the virus kills the host as soon as it is infected, because this host is less likely to transmit the virus to other people", says Barclay. Instead, simply "go for a ride" long enough to spread in coughing and sneezing. As a result, most viruses become less pathogenic over time – which did not happen with 1918.

However, more recent pandemics had already incorporated some of these adaptations before they spread worldwide. . – and as a result, they ended up being less deadly.

The 1957 pandemic, for example, occurred when an existing human virus strain acquired certain genes from a bird species. The result was a highly contagious version, but existing human components meant that it was still less lethal than a purely birdlike virus.

Similarly, in 1968, the so-called Hong Kong flu came from another "rebadembled" version of existing viruses that already contained less virulent adaptations.

The 2009 pandemic, on the other hand, was a swine flu of porcine origin – which, although not identical to humans, has characteristics closer to ours than those of birds. that is to say that it has already accumulated certain adaptations that mitigate its virulence

The study of these processes not only helps us to understand the tragedies of the past by identifying the genetic characteristics responsible for the devastating effects of the 1918 pandemic, but also to prepare ourselves to avoid such tragedies in the future.