Nurses care for victims of the Spanish Flu in tents at Lawrence, Massachusetts, in 1918
A hundred years ago, at the tail end of the First World War, a deadly new strain of influenza emerged that would infect one in three people. The ensuing pandemic cut short the lives of between 50 million and 100 million human beings. It was the greatest tidal wave of death since the Black Death of the 14th century, and possibly in the whole of human history. The 1918 flu pandemic has been studied ever since it receded in the 1920s, leaving untold misery in its wake, and though scientists know a lot more about it than they did 100 years ago, many questions remain unanswered. Why was it so lethal? Why did it attack those in the prime of life – robbing families of their breadwinners and communities of their pillars? And could such a thing happen again?
A pandemic is an epidemic that encompasses more than one continent, or as in the case of the Spanish flu, the whole world. The flu pandemic that preceded the 1918 disaster swept the world in the 1890s, killing an estimated one million people. Of the three that have struck since 1918, none has killed more than two million people, so 1918 is an anomaly that needs explaining.
Was it a coincidence that the world was at war in that year? Probably not, most scientists agree. Though the pandemic would have happened anyway, war or no war, the state of the world rendered it very much more deadly. It did so, according to current thinking, in two ways: by creating conditions that prompted the virus to ratchet up its virulence; and by disseminating the resulting microbe very efficiently around the world.
The pandemic struck in three waves, a mild first wave in the northern-hemisphere spring of 1918, a much more lethal second wave the following autumn, and a reprise in the early months of 1919 that was intermediate in severity between the other two.
‘How bad will the next pandemic be? Estimates vary from fewer than a million deaths to more than 100 million’
Between the spring and the autumn of 1918, the virus underwent a change that made it significantly more dangerous – the agent of a disease more comparable to pneumonic plague, an airborne variant of bubonic plague, than to flu as we know it.
A new virus usually moderates its virulence over time, its optimal strategy in evolutionary terms being to keep its host alive for long enough to spread it far and wide. The opposite happened over the summer of 1918, causing evolutionary biologist Paul Ewald, of the University of Louisville in Kentucky, to suggest that the unique conditions on the Western Front might have pushed the virus to pursue a different strategy.
A virus doesn’t have a strategy in the conscious sense, of course, but the genes of the viral strain that is the most successful in evolutionary terms – that reproduces the most – come to dominate in the viral population by a process of natural selection.
On the killing fields of Flanders and Champagne, thousands of young men were immobilized by being packed into trenches, meaning that the virus’s best strategy to survive and reproduce was to race through them as fast as possible, and whether it killed them or not made no difference to its evolutionary success.
The killing fields, in other words, brewed a lethal cocktail of viral genes, and the altered strain erupted in the latter part of 1918. Just as that second pandemic wave reached its peak, in November, the signing of the Armistice brought the war to an end. From then on, troops were demobilized and sent home, where they were greeted by joyous home-coming parties.
Civilians were also travelling, having been displaced from their homes by the hostilities. Therefore large numbers of people were on the move in late 1918 providing a close to ideal mechanism for disseminating a highly contagious pathogen around the world. The majority of the deaths caused by the Spanish flu occurred in the 13 weeks between the middle of September and the middle of December 1918. Of the victims, a disproportionately high number were aged between 20 and 40. More men died than women, on average – meaning, poignantly, that it wasn’t unusual for a young man who had survived the war to die of the Spanish flu – though pregnant women were also vulnerable.
Seasonal flu tends to target the very young and the very old, mainly because the human immune system takes time to mature and loses potency in old age. Why, then, did the 1918 strain target this middle age group?
A comprehensive explanation is still lacking, but one theory goes like this: a person’s immune system responds best to the first flu strain it is exposed to, with every subsequent response being a variation on that initial one and hence often a poor match for the new virus. This is because flu is constantly evolving, which in turn is the reason why the annual flu vaccine has to be updated each year.
The first strain to which many of those aged 20 to 40 in 1918 would have been exposed was the one that caused the flu pandemic of the 1890s. This was quite different from the one that caused the 1918 pandemic.
Influenza A, the type of flu that causes pandemics, is divided into subtypes according to which of two antigens – the molecules by which the host’s immune system recognizes it – the virus carries on its surface. These antigens are known by their initials, H and N. The subtype that caused the 1918 flu pandemic was H1N1, while there is evidence to suggest that the flu pandemic of the 1890s was caused by H3N8 – a different beast entirely. Another flu pandemic is inevitable. There have been around 15 in the past 500 years, with the interval between pandemics averaging 36 years, so we are due another one this century. The most recent, the 2009 ‘swine’ flu, was something of an anticlimax – in a good sense – because it killed around 300,000 people, fewer than an average flu season.
How bad will the next pandemic be? Estimates vary from fewer than a million deaths to more than 100 million – an estimate range that reflects our residual ignorance about flu, as well as the difficulty of predicting the state of the world when that pandemic erupts.
The conditions that prevailed on the Western Front are unlikely to be recreated, but we have other reasons to worry. The global population has roughly quadrupled since 1918, and our transport links are much more efficient. Yes, we have better disease surveillance, flu vaccines, antiviral drugs and antibiotics to treat the secondary bacterial infections that caused most deaths in 1918. But we also have a growing problem of antimicrobial resistance, another one of vaccine hesitancy and an ageing population.
There is no room for complacency, in other words, and come the pandemic, the best protection any of us will have will be to get vaccinated – assuming a pandemic vaccine can be produced fast enough and in large enough quantities to protect everybody, which in the current context would be a tall order.
That vaccine will probably make the difference between life and death, not only for the person who receives it, but for many of those they come into contact with. In 1918, there was no flu vaccine. But in the future, as in 1918, among the first to die will be the immuno-compromised – many of whom will catch the disease from healthier friends and colleagues who will survive.
This truth reflects the essential nature of an epidemic or pandemic. It is a collective phenomenon for which we have to prepare collectively. Seen in that light, vaccinations, the best weapon in our armoury, become something more than a personal choice, they become a civic duty.
No comments:
Post a Comment