This week, I was fortunate to find links to two scientific articles that gave me reason to think of how little we are able to understand influenza evolution and worse, how poor we continue to react and respond to such a threat.

A paper by Yamanda et al. provided us with some understanding of how the H1N1 influenza virus managed to jump species from pigs and avian species to humans.  We had originally believed that one of two particular mutations, called PB2-E627K and PB2-D701N was necessary in order to cause infections in humans (for more on the PB2 protein and influenzavirus biology in general, click here).  These mutations were in almost all human cases of the H5N1 avian flu that had so many of us concerned.  Yet these mutations apparently didn’t have the effect we expected.  Instead, there was evidence by Jagger et al. to show that these mutations decreased the impact of H1N1 infection. This was surprising in the least and led to much study to find what actually led to the species jump.

The Yamanda paper helped us understand what may have happened.  A different, relatively ignored mutation, known as PB2-Q591K led to the lethal infection in mice that was seen in severe human H1N1 infection.  While this mutation was not the one seen in the human pandemic H1N1 strain, a similar mutation, PB2-Q591R was found in the initial California strain.  As evolution goes, this mutation supported the function of the PB2 protein in the human system and allowed for stable infection and spread. Eventually, this one little mutation led to the pandemic.

The second paper from Nancy Tomes took a much different approach to the concept of H1N1.  The paper, which took a historical view of the human reaction to the Spanish Influenza pandemic of 1918-1919.  If the paper by Yamanda et al. was a shock, this put my heart into my throat.

There was practically no difference between the public measures taken then and those taken during the current pandemic.

Quarantine, social distancing, hygiene promotion, school closings and staying at home when sick were all promoted as the best activities for preventing the spread of influenza.  There were a few more radical steps taken then that were not today, such as making spitting in public a crime and admonishing those who did not use a handkerchief when coughing or sneezing.  But the majority of steps taken back then were in many ways no different than what we did over the last year to prevent the spread of H1N1.  As history will tell, the measures worked for smaller communities.  But for highly urbanized areas, the spread was almost unstoppable.  And when it came to the 2009 H1N1? Not much difference.

I admit that I’m not taking into consideration vaccination and the use of antivirals.  While these two advances have given us an ability to fight infection spread, the data suggest there was little benefit of making them available.  In terms of the 2009 H1N1 vaccine, there was less than 50% of the population who opted for the jab.  Granted, this was more a risk communication issue over a lack of interest, however, traditionally, the levels of vaccine use can be as low as 5%.  As for antivirals, the insistence that they should only be used in the most severe cases all but left the public having to fight off the virus on their own.

There is no doubt that the world of infectious disease is complex and in many ways an enigma that can lead to fear and anxiety.  The recent pandemic, no matter how mild, only highlights how vulnerable we are when it comes to these microscopic threats.  However, I don’t believe this permits us to remain inert when it comes to defending ourselves.  There needs to be a greater effort – a community effort – to better understand the impact of germs and how we can work together, even if it means through self-isolation, to keep these pathogens at bay.

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