Avian flu: this is not 1918
The discovery of a dead infected swan in Fife has led to warnings of another 1918-style flu epidemic. Let’s have some historical and scientific perspective.
The widely expected arrival of the bird flu virus in Britain has been confirmed. A swan was found dead in Fife at the end of March and revealed to be carrying the H5N1 virus last Thursday (6 April 2006). Prime minister Tony Blair urged the nation not to panic and said: ‘It is very important people understand that this is not a human-to-human virus. It is transmitted to poultry.’
That message of calm was immediately pecked at by columnists wanting to know why it took eight days to decide that the swan was infected with H5N1. Once it was reported that the swan was a mute resident of Britain, and so must have caught the virus from another bird, the talk was of Britain being complacent with the virus running loose for at least three weeks. Panic and scaremongering returned to dominance by Sunday, 9 April, as a leaked letter from Sir Liam Donaldson, the chief medical officer, revealed that all schools would close in the event of an H5N1 human outbreak. If the schools were to remain open, it was reported that 100,000 children would die, but if they were to be closed that number would be just 50,000. What was that about understanding that this is ‘not a human-to-human virus’?
Is H5N1 a threat to people in Britain or not? The one thing that everyone appears to agree on is that, right now, H5N1 is not being transmitted between humans and is difficult to catch even when coming into contact with contaminated chickens. To date there have been 191 human cases and all are believed to have followed direct contact with the fluid (blood, saliva or faeces) of an infected bird. Some scientists believe that the virus is probably difficult to catch because it embeds low down in the respiratory tract and so is not released when a person coughs or sneezes.
At the moment, therefore, the virus cannot be said to be airborne, which minimises the possibility of infection. The worry is that the virus might mutate to infect the upper respiratory tract and then become an airborne virus. Given that 108 of the 191 so far infected have died, there is reason to be concerned about an airborne version of H5N1.
There are, however, good reasons to be sceptical that H5N1 can ever mutate to infect the upper respiratory tract. H5 viruses have been known since at least the early 1980s and have been infecting humans since at least 1997. Influenza viruses mutate rapidly and H5N1 is no exception – it might even mutate more ferociously than other influenza viruses. There has been ample opportunity, therefore, for H5N1 to mutate into an upper respiratory form and, if that were possible, we might expect it to have already happened (1).
Alternatively, H5 viruses might have already mutated into an upper respiratory form. We tend to think of a mutating virus as a bad thing but mutations are random and are just as likely to have beneficial as negative effects. The virus may mutate to become bigger and more visible to the immune system, or may mutate and become less able to unload its genomic packet, or may mutate to become otherwise less virulent in human beings. Under these circumstances our immune system may be able to develop antibodies against the H5 strain with little or no illness.
Furthermore, until quite recently, it was considered almost impossible for an influenza virus to jump straight from birds to humans. This is because the receptors of the human respiratory tract differ greatly from those of birds, and so a bird virus has nothing to lock on to in the human. Human influenza viruses typically pass first from a bird to a mammal, especially pigs, that share bird and human respiratory receptors. When a pig contracts bird flu, the flu virus can mutate to attach to the human-like pig receptors. The mutated virus becomes part-bird and part-pig and can now infect humans. Thus, humans that are sick with flu most often carry a virus with pieces of genes from birds and pigs (known as a reassortment virus). Influenza viruses of type H1, H2 and H3 have all shown themselves capable of reassorting genes with mammals and caused the pandemics of 1957 (H2N2) and 1968 (H3N2).
H5 viruses were considered to be incapable of infecting mammals and thus of marginal importance in human beings until a boy in Hong Kong died of an H5 virus in 1997 that turned out to be all bird with no mammalian genes. This discovery sent shockwaves through the world of influenza science and caused panic in Hong Kong (2). The Hong Kong government bought two million doses of the antiviral drug amantadine and planned on supplying doses to all six million Hong Kong residents. Specialists from the American CDC and the World Health Organisation began arriving in Hong Kong and setting up research labs. By the middle of December eighteen people had died and there was a media frenzy. A major cull of chickens and other birds was organised and between 29 December 1997 and 1 January 1998, 1.6million birds were killed. During 1998, no further cases were reported.
Although dramatic, the 1997 outbreak supports the hypothesis that H5 is not easily transmissible to humans. The virus had gotten into humans and was epidemic in poultry. At that time, pigs, chickens and other livestock mixed freely with people in the Hong Kong market. If ever there was a place and a time when H5 was going to jump to humans and become airborne, either directly or through genetic reassortment, that was it – but it didn’t happen.
We know from history, however, that a bird virus can infect human beings without reassortment. Recent studies have demonstrated that the 1918 pandemic, which claimed tens of millions of lives, was caused by an H1N1 virus that almost certainly jumped directly from birds to humans (3). And if it happened then, goes the argument, it can happen now. It amazes me how often this argument is made without the author pausing to consider what was happening in the world in 1918.
There was a war on and the 1918 influenza piled disease upon slaughter. Surgeon George Crile wrote in his diary, ‘Everything is overflowing with patients. Our divisions are being shot up; the wards are full of machine gun wounds. There is rain, mud, flu and pneumonia.’
It is not just that the First World War was hell, which it surely was, but it was a hell uniquely designed to first create and then spread the avian H1N1 virus. Firstly, the flu did not just arrive in 1918 but had been smouldering away since at least 1915 when there were outbreaks of infectious pneumonia in German military camps and prisons. During 1915 more people died of flu in England than in any year from the previous 15. In both 1916 and 1917 there were ‘obscure but extensive febrile pneumonic outbreaks’ on both the Western and Eastern Fronts and at Aldershot military base. During peacetime these outbreaks might have been managed with medications and quarantine measures that were simply unavailable or impossible in time of war.
Secondly, there were vast numbers of people on the move. One theory is that the virus was brought in by Chinese labourers heading for Europe to work for the armies of the Western Front. Thousands were in transit across America and may have introduced new flu strains as they passed. At the beginning of 1918, America began the largest military mobilisation of its history: over 200,000 troops crossed the Atlantic during March and April. The disease arrived in India on troopships at the end of May and it moved along the railways with the soldiers, spreading throughout the subcontinent by August.
Finally, throughout 1918, when the virus was evidently infectious and lethal, thousands of young soldiers were crammed together by war – in the trenches, in camps and in transports travelling to and from them. Aggravated by impoverished shelter, a lack of food and water, limited medical facilities and cramped living conditions, the avian H1N1 virus was in an environment where it could survive to mutate into a form highly infectious and transmittable to humans. It could then readily infect vast numbers of people and move with them as they slowly traversed the globe.
Today doesn’t compare. Our health is better; our access to medicine is better and the medicines themselves are better; our shelter is better; our nutrition is better, and so on. Even our travel is better. Many commentators have argued that our access to high-speed travel means that a deadly H5N1 virus could be in Hong Kong today and London tomorrow. That is true, but not particularly important. Travelling across the globe quickly means contact with a smaller geographical area and quicker access to medical attention when it is needed. Both Hong Kong and London have excellent medical and quarantine facilities that can handle an outbreak of a deadly virus.
In summary, the H5N1 virus is currently a threat to birds but not to humans and there are good reasons to expect that situation to remain unchanged. Even in the unlikely event that H5N1 makes the jump from birds to humans there is as much chance that the jump will be harmless as it will be lethal. Finally, the worse-case scenario of the H5N1 jumping from birds to humans in a highly infective and lethal form will be bad but not apocalyptic. Because this is 2006 and not 1918, and because we do not currently face the ravages of a world war, we can expect any human form of bird flu to be contained and managed without the deaths of tens of millions of people.
Stuart Derbyshire is a senior lecturer in the School of Psychology at the University of Birmingham, England.
spiked-issue: Bird flu
(1) Yes, but will it jump?, Nature, 2006; 439: 124-125
(2) Davies P. Catching Cold: 1918’s forgotten tragedy and the scientific hunt for the virus that caused it. 1999
(3) Taubenberger JK, Reid AH, Lourens RM, Wang R, Jin G, Fanning TG. Characterization of the 1918 influenza virus polymerase genes. Nature 2005; 437: 889-893; Tumpey TM, Basler CF, Aguilar PV, Zeng H, Solorzano A, Swayne DE, Cox NJ, Katz JM, Taubenberger JK, Palese P, Garcia-Sastre A. Characterization of the reconstructed 1918 Spanish influenza pandemic virus. Science, 2005; 310: 77-80.
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