In August of 2010, roughly 16 months after the new H1N1 virus first emerged, the WHO finally declared the end of the 2009 Pandemic.
For most people the switch over to seasonal status signaled the pH1N1 threat was over.
But of course, seasonal influenza kills hundreds of thousands of people each year, and as we've seen, some seasons are much worse than others.
In the United States, the 2011-2012 and the 2015-2016 flu seasons were unusually mild (see chart above), while the years in-between were moderately severe.
The severity of flu can also be regional, as we've seen severe flu outbreaks reported in India, Eastern Europe, and the Middle East at the same time there was relatively little flu in North America (see WHO: Update On Ukraine's Flu Season).
While some of the reasons behind this variance in flu severity remain murky, two factors - the waxing and waning levels of community immunity and antigenic (and other) changes in the virus - appear to be major factors.
Although the hope is always that the longer a virus circulates in a host population, the less severe it will become, the other side of the coin is the longer it circulates, the more evolutionary changes it may acquire.
And that could not only make it more transmissible, it could make it more virulent as well.
The most recent ECDC Influenza Virus Characterization report describes pH1N1's evolution:
Since 2009, the HA genes have evolved, and nine clades have been designated. For well over a year, viruses in clade 6, represented by A/St Petersburg/27/2011 and carrying amino acid substitutions of D97N, S185T and S203T in HA1 and E47K and S124N in HA2 compared with A/California/7/2009, have predominated worldwide with a number of subclades emerging.
In other words, the 2009 H1N1 viruses of today are markedly different from those that emerged in the spring of 2009, and they continue to evolve and diversify.
Some mutations in pH1N1 - including the D225 Variant linked to more severe deep lung infection and the H275Y mutation conferring antiviral resistance - are worrisome, but are seen in fewer than 2% of samples and are not yet viewed as major public health concerns.
But today we've a study, published in Nature's Science Reports, that identifies 6 genetic changes (PA-L581M, NP-V100I, NP-I373T, HA-S202T, NA-N248D and NS1-I123V) that appeared shortly after the virus jumped from pigs to humans, and that are still seen in 99% of the pH1N1 viruses circulating today.
These changes appear to to be the result of host adaptation, are believed to have made the pH1N1 a more `humanized' virus, conferring greater transmissibility and improved viral fitness.
This study has significance beyond just pH1N1, as it suggests the longer a poorly adapted virus influenza circulates in humans (think: H7N9, H5N1, H1N1v, H3N2v, etc.), the better its chances are of adapting to human hosts.
It's a long, fascinating article, and the abstract only scratches the surface, so you'll want to follow the link to read it in its entirety.
I'll have a bit more when you return.
Evolution of 2009 H1N1 influenza viruses during the pandemic correlates with increased viral pathogenicity and transmissibility in the ferret model.
Otte A1, Marriott AC2, Dreier C1, Dove B2, Mooren K3, Klingen TR3, Sauter M4, Thompson KA2, Bennett A2, Klingel K4, van Riel D1,5, McHardy AC3, Carroll MW2, Gabriel G1,6.Abstract
There is increasing evidence that 2009 pandemic H1N1 influenza viruses have evolved after pandemic onset giving rise to severe epidemics in subsequent waves.However, it still remains unclear which viral determinants might have contributed to disease severity after pandemic initiation.
Here, we show that distinct mutations in the 2009 pandemic H1N1 virus genome have occurred with increased frequency after pandemic declaration. Among those, a mutation in the viral hemagglutinin was identified that increases 2009 pandemic H1N1 virus binding to human-like α2,6-linked sialic acids.
Moreover, these mutations conferred increased viral replication in the respiratory tract and elevated respiratory droplet transmission between ferrets.
Thus, our data show that 2009 H1N1 influenza viruses have evolved after pandemic onset giving rise to novel virus variants that enhance viral replicative fitness and respiratory droplet transmission in a mammalian animal model.
These findings might help to improve surveillance efforts to assess the pandemic risk by emerging influenza viruses.
In summary, our findings here suggest that increased vigilance in viral surveillance is required even after pandemic onset since IAV seem to harbour the potential to further evolve causing severe subsequent epidemics in the human population.
In 1957, after almost 40 years where H1N1 had dominated the global flu world, a new H2N2 virus appeared, and sparked a fresh pandemic.
The Asian flu was less severe than 1918, but more severe than 1968 and 2009, and probably killed around 4 million people.
As the chart below illustrates, intermittent severe outbreaks of that virus continued beyond the pandemic period, with H2N2 returning every few years with renewed vigor.
We saw similar spikes in H1N1 in the decade following the 1918 pandemic, with peaks reported in 1923, 1926 and 1929 (see The Pandemic Influenza Enigma).
While we are always on watch for a novel flu to appear, sparking the next pandemic, history has proven time and again that sometimes even an old flu can learn new tricks.
So we watch for changes in both of our seasonal influenza A viruses, always mindful that either of them could produce a particularly nasty flu season down the road.