An influenza smiley

What is this swine H1N1? Pigs are known hosts for all kinds of different influenza viruses, including human and avian varieties. They are often depicted as ideal “mixing vessels” for influenza, where all types of different influenza viruses can mix together with the potential to form new combinations – a reservoir for emerging viruses. The H1N1 genes code for the surface glycoproteins of the virus and are the main target of the immune response. The present virus's H1N1 genes are predominantly porcine in origin, but they also contain pieces related to human and avian influenza viruses and thus represent a previously unknown subtype. Human and porcine H1N1 viruses are close relatives but, thanks to a number of differences distributed along the genome, they can be easily distinguished. These differences cause subtle phenotypical changes resulting in either specific adaptation to swine or humans or, for some, in the potential ability to cross the species barrier. After a time period of unknown duration in swine, the present H1N1 virus has just crossed this barrier, and by so doing, in contrast to the H5N1 avian virus, it has also acquired the ability to be transmitted by respiratory droplets between humans and to establish a human reservoir. A question mark remains: why was this virus not previously identified in surveillance systems in animals? Identification of the initial animal reservoir may only be a question of time: H1N1 has recently been identified in Canadian pigs. However, given the very rapid pace of events, we need more observations and epidemiological data before definite conclusions can be drawn. Fortunately, at the moment, the virulence of the virus seems to be limited and at worst similar to severe seasonal human influenza. Again, this is not certain, and the observed mortality in Mexico is disturbing. The age distribution of hospitalised cases is also peculiar, since the median age seems to be approximately 15 to 20 years. We must also bear in mind that most proven cases in the United States or Europe have been treated by neuraminidase inhibitors, an intervention that may change the course of the disease and prevent complications. At present we have a flood of incomplete information and few evidencebased conclusions. Hints do not equal proof. The pessimists will say “Yes, the mortality is low, but given the virus's capacity to mutate it might well become more virulent”; but the opposite could also easily occur and there are no scientific reasons at present to make assumptions either way. Since the virus was isolated only a few weeks ago, our knowledge of it is still limited. Animal models, in vitro studies etc. are lacking. Two points are not presumptive, however: the first is the fact that the strain is sensitive to neuraminidase inhibitors, the only antiviral agents available against this virus; and the second is that only one mutation can lead to resistance. This has already occurred in the human H1N1 virus, in the absence of strong selective drug pressure. Given the number of oseltamivir pills distributed recently, the rapid emergence of resistant strains will not be surprising (and may indeed even be expected). Another issue is the immune response. It appears that the current H1N1 vaccine affords no protection against this new swine strain, but whether previous H1N1 infection with other natural strains could provide some kind of protection requires investigation. Certainly the present outbreak will complicate the design of new vaccines. In addition to the usual human

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