Swine Flu Editorial: Journal of Biology

Influenza: digit or two more questions

Miranda Robertson Journal of Biology 2009, 8:45doi:10.1186/jbiol158
The electronic version of this article is the rank digit and crapper be found online at: http://jbiol.com/content/8/5/45
Published: 12 June 2009 © 2009 BioMed Central Ltd

Editorial

When we asked saint Doherty to write a question-and-answer piece on contagion [1], Australia, where he is based, had digit reportable case of contagion A (H1N1). At the instance 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 take at which the host survives to become reinfected (or to produce young that become infected). The most notable example of such adjustment is in the herpesviruses, which hit evolved a quite exceptional aggregation of devices for avoiding manlike status and with which most manlike adults in the Western concern are chronically infected. Herpesviruses persist through latency. Influenza virus belongs to a different strategic class, which proliferates apace and escapes in coughs and sneezes, leaving the host immune. Most humans survive infection with manlike contagion viruses; but the adaptive peace may break down when the manlike viruses recombine with viruses of avian or swine origin: hence the high manlike mortality associated with the H5N1 avian contagion virus that emerged into public knowingness in 2005. The so-called swine H1N1 contagion virus that is the drive of the current pandemic is apparently a triple-reassortant, with genes of swine, manlike and avian origin. Unlike H5N1 it is readily transmissible between humans, but it seems - so far at least - otherwise inferior uncouth, and in most grouping causes only temperate disease; so perhaps in respect both of transmissibility and of pathogenicity it reflects its manlike kinda than its swine or avian origins. What makes this virus particularly dangerous, as saint 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 contagion immunogen programme.

It is probably the take - or kinda the distribution - of population status that also partly accounts for the atypical pattern of mortality of pandemic as against the usual seasonal influenza. Whereas seasonal contagion is more probable to kill the old, pandemic contagion (including the present H1N1 influenza) tends preferentially to kill the young. This is intellection to be because senior individuals are probable to hit some take of status cod to crossprotective antibodies - that is, antibodies against similar features of other, in this case past, contagion viruses. (I ought however to restate that disease cod to contagion A (H1N1) seems generally mild; and indeed mortality is almost certainly even modify than it seems, because it is highly probable that some pussy individuals never bother to consult a doctor and the number of grouping actually pussy thence probably substantially exceeds the number reported.)