Paris, April 21: There may be many people who believe that as its first anniversary looms, this is a great moment to consign swine flu to the Book of Great Health Scares.
To them, virologists sound a word of caution.
Yes, they admit, rather chastened, the novel virus did turn out to be less nasty than many predicted.
Possibly hundreds of millions have been infected by the bug, officially known as 2009 H1N1 influenza, since it was officially notified on April 24 last year.
But less than 18,000 have been killed by it, according to the UN’s official death toll.
That places it in roughly the same ballpark of lethality as a routine, or “seasonal,” flu virus.
H1N1 thus bears no comparison to fellow pandemic viruses that erupted in the last century. These strains scythed as many as 50 million lives in 1918-19 and one or two million each in 1957-8 and 1968-9.
Even so, say these and other experts, H1N1 still has devastating potential and the world must maintain its guard.
“In the past, more often than not, the first wave (of a flu pandemic) has been overshadowed by the second and third waves,” says John Oxford, a professor at Queen Mary’s School of Medicine and Dentistry in London.
Lone Simonsen, an epidemiologist at George Washington University, notes that in the 1968-9 pandemic, about 70 percent of the fatalities occurred in the outbreak’s second year.
The theoretical underpinning of this thinking is Darwinian tradeoff.
In its early phase, according to this hypothesis, a new virus finds it easy to survive because billions of people have no, or at best limited, immunity to it.
But this pool of easy pickings dwindles, which means the virus has a harder time finding a human host. To survive, it has to devise a new foothold.
That means genetic change: the virus changes shape through mutation or trades some of its transmissibility in exchange for greater lethality by picking up genes from nastier flu viruses.
As for mutation, very little variation has been seen in the present pandemic strain of H1N1, says virologist Albert Osterhaus of the Erasmus Medical Centre in Rotterdam.
It is likelier to drift genetically, as “seasonal” strains do, rather than leap.
That is good news for vaccine campaigners. People who were infected by H1N1 or primed with the anti-H1N1 vaccine are likely to get a lot of carry-over immunity for the 2010-11 flu season.
Of greater concern, says Osterhaus, is the risk of a gene mix, or reassortment, with other flu viruses.
He points to countries where H1N1 co-circulates with H3N2 strain and the notorious H5N1 strain of bird flu, which carries a case fatality rate of some 60 percent.
Osterhaus also voices worry over another genetic risk: the possibility that H1N1 widens a so far rare resistance to oseltamivir.
This drug, also called Tamiflu, is the frontline treatment for flu. It is not a cure, but if taken early enough can reduce viral numbers, thus reducing contagiousness and shortening the length and severity of illness.
Overall, the news today is reassuring.
But given the uncertainties, watchdogs will need to prepare an arsenal of options when the 2010-2011 flu season returns in the northern hemisphere’s autumn, says the European Centre for Disease Prevention and Control (ECDC).
Epidemiologists will be keeping a close look at the southern hemisphere’s winter, from June-September, to see if there is any data that points to a change in target or lethality by the virus.
The 2010-2011 vaccine campaign will have to fine-tune recommendations for shielding groups most at risk and concentrate on “countering anti-vaccine messages and campaigns” that scared many people into refusing the jab, says the European Society of Clinical Microbiology and Infectious Diseases (ESCMID).
–Agencies