Ok, not really right now. As of the end of October, the rates of Influenza-like Illness has been gradually increasing, with the Centers for Disease Control reporting that “sporadic” rates of laboratory confirmed influenza have been found here in Pennsylvania. These numbers will continue to rise over the next few months as the disease continues to follow its typical seasonal course. The typical “flu season” begins at the start of winter, right around Week 50 or so, and goes through about Week 10 in the new year, and the peaks visible in this graphic from the CDC show the significant 2007-2008 season, followed by the somewhat milder 2008-2009 season. The big peak between weeks 30 to 50 (mid summer to late fall) in 2009 was the pandemic H1N1 flu outbreak, with the anticipated seasonal flu outbreak appearing as the smaller shoulder on the graph next to the big peak.
My new issue of Microbe magazine came in the mail today, and I was reading this afternoon. There was a fascinating article on what we’ve learned about the 1918 influenza pandemic virus. The DNA sequence of this isolate of the virus has been constructed by examining formaldehyde fixed tissue samples from people who died during that epidemic, and that knowledge has taught us a lot about the lethality of that virus epidemic. What are some of the things we have learned about this virus? One issue that influenza virus has to face in the process of infecting a human cell is that it has to leave an infected cell after it multiplies. This will allow the virus to spread the infection. Experiments using human airway cells have shown that these cells release 50 times more of the 1918 virus in comparison to modern influenza viruses. This means that the infection would potentially spread more quickly. The highly pathogenic 1918 virus also appeared to be more effective at infecting the lower respiratory tract of humans. This is an interesting contradiction to the 2009 pandemic, which was highly contagious (the CDC estimates now that 50 million Americans were infected last year, resulting in 200,000 hospitalizations and 10,000 deaths,) but was not associated with the high mortality of the 1918 pandemic. In fact, if you run the numbers in the previous sentence, the 2009 pandemic had a mortality rate of only 1 in 5000 infections, or 0.05%, despite both the 1918 strain and the 2009 strain being the H1N1 type. So it appears that the ability to infect the upper airway (something that 1918 and 2009 have in common) is important for the communicability of the virus, but the ability to infect the lower airway is important in the pathogenesis of the disease. The complete virus determinants which dictate this ability are not known, but are the topic of many research labs.
Now to get a second flu shot, just in case!