For the last couple of decades, perhaps beginning around the time of the publication of Laurie Garret’s excellent thesis (The Coming Plague: Newly Emerging Diseases in a World Out of Balance) on disease and politics and continuting through Gina Kolata’s “Flu: The Story Of The Great Influenza Pandemic” there has been increased attention on the 1918 flu virus and pandemic, as well as subsequent outbreaks. This interest has probably been fueled by increased knowledge of (or incidence of?) tragic and highly newsworthy outbreaks of Ebola, SARS, and so on. More recently, the perception has grown that the Bird Flu is a’comin’ any time now to ultimately replace the Great Pandemic of 1918 as well as the mud shark in our mythology.

If you read the better done public-oriented literature of this period, you will learn that the nature, cause or origin, and pattern of the 1918 epidemic has been very mysterious. The same level of mystery (but with only a few victims) arose in connection with the Swine Flu threat of the 1970s (see expecially Garret’s book for how this event links to current attitudes as well as public policy regarding vaccines).

This brings us to some time last year or so, when key papers were published (and I presume presented at conferences) regarding what may ultimately be seen as the most important single step in the history of understanding the way the flu vaccine works, and thus, how to combat it. (See this to explore one of those key moments in research history.)

The new knowledge is essentially an improved evolutionarily and developmental understanding of how influenza virus strains change over time. To put it very simply, these viruses are made of chunks that come apart in the host and then recombine. If there are multiple ‘strains’ (think species, more or less) of influenza in an individual, these genetic chinks, each representing a huge percentage of the influenza genome, can and do re-combine to form entirely new strains.

That is in a sense macro-evolution of a pathogen in situ, in the host. What is an immune system to do!?!!?!?? Not much, really. This can be very fatal.

It is now understood that these epidemic or pandemic influenza outbreaks arise from these recombination events. If you now look back at the quirky data, the odd logic influenza seemed to be patterned by, the epidemiological dead ends that seemed to confound everyone through the lens of knowledge of these genetic chunks, called “reassortants,” things suddenly become much much clearer.

A paper has just come out in PNAS reporting research using a primate model to explore immune response and associated pathology under the influence of a recombinant influenza virus, and this research is a direct outcome of this new way of looking at the flu. I offer it here without comment largely because you can get the article yourself, since this one is an OpenAccess piece from the normally not OpenAccess PNAS. Here.

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