Influenza: one or two more questions
Journal of Biology 2009, 8:45doi:10.1186/jbiol158
The electronic version of this article is the complete one and can be found online at: http://jbiol.com/content/8/5/45
| Published: | 12 June 2009 |
Editorial
When we asked Peter Doherty to write a question-and-answer piece on influenza [1], Australia, where he is based, had one reported case of influenza A (H1N1). At the time of writing this editorial, Australia has more than 1,200 cases (though to date no deaths) and has triggered the announcement by WHO of a global pandemic.
Received wisdom has it that pathogens are not generally lethal to the hosts they normally infect, because they could not survive if they were. Pathogenicity thus becomes adapted to a level at which the host survives to become reinfected (or to produce young that become infected). The most notable example of such adaptation is in the herpesviruses, which have evolved a quite extraordinary repertoire of devices for avoiding human immunity and with which most human adults in the Western world are chronically infected. Herpesviruses persist through latency. Influenza virus belongs to a different strategic class, which proliferates rapidly and escapes in coughs and sneezes, leaving the host immune. Most humans survive infection with human influenza viruses; but the adaptive truce may break down when the human viruses recombine with viruses of avian or swine origin: hence the high human mortality associated with the H5N1 avian influenza virus that emerged into public consciousness in 2005. The so-called swine H1N1 influenza virus that is the cause of the current pandemic is apparently a triple-reassortant, with genes of swine, human and avian origin. Unlike H5N1 it is readily transmissible between humans, but it seems – so far at least – otherwise less uncouth, and in most people causes only mild disease; so perhaps in respect both of transmissibility and of pathogenicity it reflects its human rather than its swine or avian origins. What makes this virus particularly dangerous, as Peter Doherty and Stephen Turner explain in their Q&A in this issue of Journal of Biology [1], is simply that most of us are not immune to it, and it was not, until now, on the agenda for inclusion in the seasonal influenza vaccine programme.
It is probably the level – or rather the distribution – of population immunity that also partly accounts for the atypical pattern of mortality of pandemic as against the usual seasonal influenza. Whereas seasonal influenza is more likely to kill the old, pandemic influenza (including the present H1N1 influenza) tends preferentially to kill the young. This is thought to be because older individuals are likely to have some level of immunity due to crossprotective antibodies – that is, antibodies against similar features of other, in this case past, influenza viruses. (I ought however to restate that disease due to influenza A (H1N1) seems generally mild; and indeed mortality is almost certainly even lower than it seems, because it is highly likely that many infected individuals never bother to consult a doctor and the number of people actually infected therefore probably substantially exceeds the number reported.)