We have just been visited by the third wave of a classical super fit, dominant and very Darwinian pandemic virus. In fact Charles Darwin would find it incredible to view his own theory of survival of the fittest proved before his very eyes in one year.
Every virologist was taken by surprise when this new influenza virus came to our notice in April 2009.
The virus spread quickly and within weeks cases were appearing in the UK. Early summer outbreaks built up in Spain and the USA. The original virus was mild but with a sting in its tail, and here we come to the crux of the matter that explains the winter outbreak we have just experienced in the UK.
Two serological analyses, one in London and the other in Edinburgh, searched for evidence of total clinical and subclinical infections in the first wave. We had all suspected that many victims had no symptoms at all. The laboratory tests, albeit from only a few thousand sera, showed in excess of a third of young people sero converted in the summer and autumn waves of 2009.1
There was a view by some that influenza A H1N1 would not revisit this winter and so the precautions of the preceding year - adverts for hand disinfection, vaccination of under five-year-olds - were lowered. But a truly Darwinian virus takes little note of one-third of the population having been infected already. After all, two-thirds remain susceptible.
The young 'at risk'
There is a further very crucial consideration: a Darwinian virus dominates and will push aside other influenza A viruses. Influenza A H1N1 targets the young, and especially the young 'at risk', including pregnant women whose immune system is somewhat dampened during pregnancy.
It was soon obvious that anyone over the age of 65 had some prior immunity, presumably from a cousin virus of the H1N1 family circulating in the 1940s and 1950s, when once again the H1N1 virus family was dominant. So for two years now the elderly, normally the target of influenza, and where mortality usually arises, have been relatively free of infection. The H1N1 virus cannot infect them and other influenza A viruses such as H3N2 have been pushed aside.
However this year, as usual, the over 65s were the target of the influenza vaccine campaign, although by December ominous signs were afoot. Influenza A H1N1 had returned to claim the two-thirds of the younger population who were still susceptible and the influenza-like illness figures began to mount. We are fortunate that influenza A H1N1 lacks full virulence punch, but nevertheless mortality began to increase.
What happened this year?
At least a third of young victims had no prior underlying illness: we knew this right from the beginning of the outbreak more than a year before and this presented a worrying combination for GPs.
By Christmas, the virus was in epidemic proportions in the under five-year-olds (circa 200 influenza-like illness cases per 100,000 people in the population).2 Usually in the family, the centre of most influenza activity, the virus is introduced by the child at play group, where poor hygiene and physical closeness allows influenza A to thrive.
The virus then moves to the older siblings, and on to the parents and finally to the grandparents, for whom it may be fatal. But as we noted above, this year the grandparents stayed well. Most vaccines had been distributed by December to the grandparent sector leaving too little for the under five-year-olds.
Under heavy pressure, supplies of stockpiled monovalent H1N1 vaccine were released in the UK but this was done rather late in the season.
Behind the mortality figures
Unfortunately young people are still dying of this virus with a total of 439 deaths between October 2010 and February 2011 and at the peak more than 700 young people were in intensive care.
As usual with influenza, the virus did not strike equally in the UK but spread in London before moving to the northern and central areas of the UK. During these three waves death rates, particularly in children, varied, with a higher rate in ethnic minorities.
This is unlikely to be driven by genetics and more likely by poorer infrastructure in immigrant areas. The recent serological data also suggests higher influenza rates in disadvantaged regions.
From the very beginning of the pandemic respiratory physicians noted that infections from this virus could be very deep-seated in the lung. Experimental virologists confirmed this in laboratory models of ferrets, mice, guinea pigs and primates. But from a public health viewpoint the vaccine was remarkably effective at preventing hospitalisation, while the rapid use of oseltamivir was most crucial in preventing pneumonia.
The third arm of our defence zones, hygiene and social distancing, has also been shown to add to our protection. In fact the three zones can be synergistic. So far the virus has not mutated to become resistant to oseltamivir or to become more virulent and has not changed antigenically.
I would predict that, by next year, influenza A H1N1 will have settled a little and will become less dominant. This could leave the population to be infected simultaneously by influenza A H3N2 and B in the elderly, while H1N1 still affects the youth.
I hope that GPs will be able to vaccinate more of the 'at risk under fives', and younger sectors. Equally importantly, I hope they are allowed the time to vaccinate themselves and their own nursing and administration staff and family members.
- Professor Oxford is professor of virology at Barts and The London School of Medicine and Dentistry, Queen Mary, University of London
- Declaration of interest: none
1. Hardelid P, Andrews NJ, Hoschler K, et al. Health Technol Assess. 2010; 14(55): 115-92.
2. RCGP. Communicable and Respiratory disease report for England and Wales. www.hpa.org.uk/hpr/infections/RCGP_Graphs.pdf