Influenza: one or two more questionsMiranda Robertson 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 © 2009 BioMed Central Ltd
EditorialWhen 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.)

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Posted By Jeff Sutherland to Dr. Jeff Sutherland's Electronic Medicine
at 6/13/2009 04:33:00 AM