Most encounters between man and microbe are of an intermediate sort. A flu virus arrives which is related to one that was around three years ago, and to which a proportion of the population has partial immunity. The upshot of this situation is very difficult to prophecy. Among other factors, it will depend upon the virulence of the virus, the ease with which it is transmitted from person to person, and the strength of the immunity in the human population.
In spite of these uncertainties, however, there are some very clear general guidelines. Waves of influenza A come to plague us roughly every two or three years, and outbreaks vary from a few isolated cases to epidemics that quickly involve 10 per cent or more of the population. Influenza B, which travels less quickly though the community, causes epidemics every three to six years.
Asian flu was a typical example of a new virus (labelled A) against which most of us were defenceless. Although the illness was generally mild, there were about 80 million cases of Asian flu. It spread at a remarkable rate and soon became disseminated widely throughout the world after originating in China in the spring of 1957. Within six months, there was a pandemic – a world-wide epidemic. Major changes of this sort in influenza A viruses occur about every 10 years, and the next such pandemic was that of Hong Kong flu in 1968.
In modern times, of course, air travel greatly facilitates such transmission. The earlier, catastrophic pandemic of 1918-19 moved rather more slowly, though its eventual toll was about a billion people – roughly half of the world’s entire population. Twenty million people died as a result of the 1918-19 pandemic, some as a result of pneumonia caused by the virus itself, some following secondary complications produced by bacteria.
There is no cross-protection whatever between A and B viruses; immunity against either type confers no resistance against the other. Within each group, however, there is some cross-protection. Antibodies formed in response to infection against one A strain, for example can afford some resistance against a related A strain. It is, of course, only during sizeable epidemics that the medical authorities usually have a detailed picture of which viruses are circulating and causing trouble. Indeed, many of the vague illnesses that we tend to label as flu may well not be influenza at all, but respiratory infections caused by other viruses and bacteria.
The variability of flu viruses is frustrating for vaccine manufacturers, who have a constant struggle to keep up with the new varieties. A vaccine that was highly satisfactory in conferring immunity against an epidemic strain last year may have little or or no value in forestalling the ravages of this year’s major villain. It is very difficult to isolate a new virus, in the Far East, say, and use it to produce a vaccine quickly enough and in sufficient quantities to immunise those who want or need it by the time the epidemic wave arrives in Britain.
All manufacturers can do is to ensure that their vaccines contain ingredients effective against most of the recently circulating strains. Attempts are, however, now being made to exploit those same processes of periodic change which flu viruses undergo in nature, to tailor-make potent vaccines more rapidly when novel variants do arise.
This season in Britain, we have seen moderate epidemics, particularly in London and the South-east, caused by two different A viruses (one of which originated in New Guinea last November) and by a B virus that appears to have caused more intestinal upsets than is usual with flu. Very recently too, microbiologists have become greatly concerned about the re-emergence, among young soldiers at Fort Dix, New Jersey, of an A strain closely related to, if not identical with, the one responsible for the 1918-9 pandemic. It seems that this virus, which is also virtually indistinguishable from that which produces swine influenza, may have been maintained ever since in pigs, until being transferred once again to humans.
What we do know is that antibodies against this virus can be found only in the blood of people old enough to have been infected in 1918-9. For the moment, the hopes are that because we are better nourished and because we now have antibodies to cope with bacterial complications, any epidemic triggered by this virus would be nothing like as severe as the earlier pandemic. But, as we have seen, predicting the ravages of flu is fraught with uncertainty.
