Why the flu of 1918 was so deadly

Why the flu of 1918 was so deadly

If you're reading this article, you've probably been through at least one global influenza pandemic – one as contagious as the deadly burden of 1918. There was the outbreak of 1957 (the so-called "Asian flu") and the "Hong Kong flu" in 1968. Forty years later, in 2009, there was the "swine flu".

Each pandemic had similar origins, which in one way or another evolved from an animal virus that developed between humans. The death toll was hardly comparable. It is estimated that between 40 and 50 million people died from the burden of 1918 – compared to two million for the influenza from Asia and Hong Kong and 600,000 for the swine flu 2009, both of which had a mortality rate of less than 1%.

The human costs of the 1918 pandemic were so high that many doctors continue to call it the "greatest medical holocaust in history." But what made it so deadly? And could this knowledge help us prepare for a similar pandemic today?

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An understanding of these pandemics would not be possible without the recognition of the great leaps in medicine in the 20th century. Doctors had only discovered the existence of viruses in 1918. "And they certainly did not know that this is a virus that causes these diseases," says Wendy Barclay of Imperial College London. They were far removed from the antiviral drugs and vaccines that can now help curb the spread and promote faster recovery.

Many flu deaths are also caused by secondary bacterial infections that root in the weakened body and cause pneumonia. Antibiotics such as penicillin, discovered in 1928, now allow doctors to reduce this risk, but in 1918 there was no such treatment. They also had no vaccines that now help protect the most vulnerable. "Our healthcare infrastructure and diagnostic and therapeutic tools are much more advanced," said Jessica Belser, who works in the influenza department of the US Centers for Disease Control and Prevention.

Apart from the lack of basic medical devices in 1918, deaths were also a direct result of the appalling living conditions of that tragic period in human history. The trenches would have been the perfect breeding ground for infections among the soldiers of the First World War. "The virus was created when populations that previously had little contact were brought together on the battlefield," says Patrick Saunders-Hastings of Carleton University in Ottawa. "And in many cases, these were other malnourished injuries." In particular, vitamin B deficiency has been found to increase the mortality rate in later pandemics, he says.

Even those left behind at home still lived in closed, overcrowded conditions, leading to more infection with the virus. This not only accelerated transmission but also increased the likelihood that humans would become infected. It also increased the severity of the symptoms. "We know that the greater the dose that penetrates you, the sicker you become, because the virus can overpower the immune system and get your body under control," says Barclay.

"It is well known that improved sanitation and sanitation, combined with industrialization and general poverty reduction, have contributed significantly to reducing infectious mortality in the 20th century," agrees Kyra Grantz of the University of Florida. In analyzing Chicago records during the 1918 pandemic, she has shown that factors such as population density and unemployment directly influenced a person's likelihood of developing the disease.

Interestingly, the Chicago data also showed a strong correlation between mortality risk and illiteracy rates in different regions of the city. This may be due to the fact that illiteracy was merely a guide to other poverty-related factors. However, it is possible that the lack of education of a person has also played a direct role in the progression of the disease.

When the techniques for capturing, storing, cultivating and analyzing viruses were invented, the original deadly burden had long since disappeared

"There has been a tremendous effort by public health officials to stop the Chicago outbreak, including quarantine across the city, school closures, and banning certain social gatherings," says Grantz. "These actions will only be effective if people are aware of it and stick to it."

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

When the techniques for capturing, storing, cultivating and analyzing viruses were invented, the original deadly burden had long since disappeared. Recent advances in genome technology have now enabled scientists to revive an active virus from blueprints of inert historical samples that have infected laboratory animals like monkeys to study their effects.

In addition to the very rapid replication, the strain 1918 appears to trigger a particularly intense response of the immune system, including a "cytokine storm" – the rapid release of immune cells and inflammatory molecules. Although a robust immune response should help combat infections, an overreaction of this type can overburden the body, leading to severe inflammation and fluid retention in the lungs that can increase the likelihood of secondary infections. The cytokine storm could help explain why young, healthy adults, who usually find it easier to shake off the flu, were the worst affected, as their stronger immune system triggered an even stronger cytokine storm in this case.

To understand why the tribe of 1918 had this effect, we must return to its origins.

It is believed that the flu of 1918 has only just developed from a strain that typically infects birds – mutations that allowed it to infect the upper respiratory tract. This meant that it could be more easily transmitted through coughing and sneezing through the air.

It is not good for the virus to kill the host as soon as it is infected, as this host has a chance to pass the virus on to other people – Wendy Barclay

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

Equally important, however, was that the virus itself was not fully adapted to life in the human body. Contrary to expectations, it is usually not in the interest of an influenza virus to kill the host. "It's not good for the virus to kill the host as soon as it's infected, because this host has a chance to pass the virus on to other people," says Barclay. Instead, it just has to be taken long enough to spread through coughing and sneezing. As a result, most viruses develop to less pathogenic overtime – but the 1918 virus had not yet made these adjustments.

In contrast, the later pandemics had already made some adjustments before they spread around the world – and were thus less deadly.

For example, the 1957 pandemic arose when an existing human strain of the virus received some genes from a bird species. The result was a very contagious strain, but due to the presence of human components it was even less deadly than a virus that comes purely from the bird world. Similarly, the so-called 1968 Hong Kong Flu came from another "re-sorted" version of existing viruses that already had the less virulent adjustments.

The 2009 pandemic was a swine flu that came from pigs – which, although not identical to humans, are closer to us than birds, meaning that they had already made adjustments that mitigated their virulence.

Studying these processes not only helps us to understand tragedies of the past. By identifying the genetic characteristics responsible for the devastating effects of the 1918 pandemic, we may be better prepared to prevent similar tragedies in the future.

"In my view, more information about test pandemic viruses can help guide our decision-making and knowledge, and show how we can best address future pandemic threats," says Belser.

David Robson is a senior journalist at BBC Future. He is @d_a_robson on twitter.

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