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If you read this story, you have probably had at least one global influenza pandemic, a disease as contagious as the deadly strain of 1918.
The 1968 epidemic spread rapidly worldwide, infecting more people than the 1918 flu – but causing far fewer deaths
Photo: Getty Images / BBC News Brazil
The outbreak of 1957 (known as Asian flu) and that of Hong Kong took place in 1968. Forty years later, in 2009, it was the turn 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 with 2 million in Asia and Hong Kong, and 600,000 in swine flu, both deaths 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. There were also no antiviral drugs or vaccines that could now help stop its spread and speed up the patient's recovery.
Many influenza deaths 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.
Robust Defenses
"Our health infrastructure and diagnostic and treatment tools are much more advanced today," says Jessica Belser, who works at the US Department of Influenza's Department of Influenza. 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 decline in poverty have largely contributed to the reduction of mortality by infectious diseases in the twentieth 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.
Since 1918, many companies have developed medical services and much more advanced public health campaigns that could stop the spread of epidemics.
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 authorities have made considerable efforts to end the epidemic in Chicago, including some 40 throughout the city, the closure of schools and the banning of agglomerations "said Grantz. "But these measures are only effective if people understand why they are caught and adhere to them"
Extreme Case
Despite these factors, many scientists believe that the virus itself was also particularly violent – although 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 quickly, the strain of 1918 seems to trigger a particularly intense reaction of the immune system, including rapid release of white blood cells and inflammatory molecules.
Although a strong immune response can help us fight the infection, such an exaggerated reaction can overwhelm the body, resulting in severe inflammation and fluid build up in the lungs that can increase the risk of developing the infection. 39 secondary infections.
This "immune storm" may help explain why young, healthy adults – who usually recover from a faster flu – have been the most affected, as their defense systems are more powerful.
Origins
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.
Contrary to what many people think, it is not in the interest of a virus to kill its host.
"It's not good for the virus to kill the host as soon as it's infected, because that host is less likely to spread 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 – but this did not happen with 1918.
On the other hand, subsequent pandemics had already incorporated some of these adaptations before they spread all over the world – and thus ended up being less deadly.
The 1957 pandemic, for example, occurred when an existing human virus strain acquired some 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 already carrying less virulent adaptations.
The 2009 pandemic was a swine flu of porcine origin – which, although not identical to humans, has characteristics more similar to ours than those of birds. That is, that it has already accumulated certain adaptations that mitigate its consequences. virulence
The study of these processes helps us not only to understand the tragedies of the past, to identify the genetic characteristics responsible for the devastating effects of the 1918 pandemic, but also to prepare ourselves to avoid similar tragedies. 39; future.
"From my perspective, having more information on pandemic viruses in the past can help guide our decision-making and knowledge, as well as best guide the management of future threats." ", concludes Belser.
BBC News Brazil – All rights reserved. Reproduction is prohibited without the written permission of BBC News Brazil.
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