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Map of Queensland's Hospital and Health service
areas. Adapted from
Click on image to enlarge.
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"Woopty Doo" some, perhaps very few, of you said. "That number means nothing until you look back at it later".
So, let's look back at it now that it's later.
It was Autumn then and now its Winter which is Flu season and also the season when we get some more public info on a handful of other respiratory viruses circulating here in Queensland thanks to the collatory (I don't care if a dictionary doesn't recognize it) genius of the crew at the State of Queensland, Queensland Health (SoQ|QH).
So what's happening with flu Down Under? For all the detailed detail, I recommend you check out the Open Access document, Statewide Weekly Influenza Surveillance Report that spans up to Week-23 (that's the week ending 8-June; we're in Week 25 now)
Turns out its still 2x (well, 1.987x but who;/s counting?) above the 5-year-to-date mean. No, this is not a "I told you so" - just that it's interesting to see that on this occasion at least, autumn trends predicted a winter event. Still, its only early winter. We've also had a very warm and dry autumn (see the Bureau of Meteorology for more on Autumn) for those who like to link weather and influenza activity.
I like to look at virus interactions as driving their own seasons. How is that possible I eerily hear you ask (I'm not listening to the "Oh what a load of..." comments by the way, so sit back down and put up your hand)? Well, they don't do anything themselves of course, but my theory goes like this...
When there are enough of us in the community infected by one virus (say respiratory syncytial virus [RSV]) and our immune-thing-a-me-whats-it is all fired up and producing an inflammatory response to rid us off said pestilence, that responsey thing offers a kind of "Shield's Up" effect.
For a short while we feel like rubbish but we also don't let other viruses get in as easily because we're in an "antiviral state". Enough of us in that state and we get a kind of short-term herd immunity (a fairy died) - where the number of people fully susceptible to another virus (say, an influenza virus) is too small for it to get a good toehold in us and the population. This pattern among seasonal respiratory viruses is most often observed, in my experience, for viruses with an RNA genome like RSV, rhinoviruses and influenza viruses.
Thankfully for my hypothesis, the data from SoQ|QH show a nice example of this pattern of viruses interacting with viruses within us, projected to the level of the community.
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A snippet from the State of Queensland, Queensland
Report for 1-January-2014 to 8-June-2014.
Edited by Ian M Mackay, VDU.
Click to enlarge.
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Part A shows the notifications for influenza viruses in Queensland. Peaks and troughs, As and Bs. Cool
Part B shows some of the respiratory viruses, including RSV which has been having a bonza season this past autumn by the looks of things.
Can you see the pattern?
Part C is a cobbled together composite I made in Photoshop/Illustrator by laying B over A and making B partly transparent. It's a bit rough and has had the axis labels and legend trimmed off for clarity, but it makes the point. What it shows (to me anyway) is that when RSV numbers go up, influenza virus notifications head downwards.
Is this due to RSV influencing influenza or influenza exerting its muscle on RSV? Can't tell from this sort of analysis.
The fact that RSV can rise in the presence of influenza virus may speak to its dominance. But take a step back. Remember we're taking about people not cells in a dish. It may be that 2 distinct populations are at play initially; perhaps younger children with RSV versus older children and adults with influenza. Once infected people reach a critical mass, that virus may win out and "push put" the other.What's happening in a single household - kids bringing home one virus, parents another perhaps? That would be intriguing to know with these concepts in mind using molecular methods and longitudinal regular sampling of whole families, regardless of symptoms.
Statistically, when I've looked at this with other data, that negative association, more obvious and frequent between influenza virus and rhinoviruses, does reach significance. You can read one of my group's hospital-based studies in [4] and a collaborative community study in [5]. Rhinovirus seasons usually bracket influenza season. So I offer a different view of how seasonal viruses are seasonal. With the sources of variability I discuss above as well as genetics and differences in everyone's past virus exposures and immune-thing-a-me-whats-it status to each virus, some cross-protective, some not, some having got really sick last year, some not...its not hard to see how those virus seasons can shift around from year to year as well.
Yet another reason to test for viruses, and to include more than just 1 or 2 viruses in that testing; the more you test, the more you can observe and learn.
By the way, interferon-the major player in causing these virus:virus interactions, got its name because it could block a secondary viral infection much like those that I've described above, but on a population level.
Now, try and get some funding to do any research on that. I hate you if you do by the way (yes, I failed miserably).
References...
- Statewide Weekly Influenza Surveillance Report, 1-January to 8-June 2014.
http://www.health.qld.gov.au/ph/documents/cdb/influenza-qld-140101-140608.pdf - Queensland in autumn 2014: A warm autumn; coastal rainfall but dry inland of the Great Dividing Range
http://www.bom.gov.au/climate/current/season/qld/summary.shtml - Do rhinoviruses reduce the probability of viral co-detection during acute respiratory tract infections.
http://www.ncbi.nlm.nih.gov/pubmed/19376742 - Community-wide, contemporaneous circulation of a broad spectrum of human rhinoviruses in healthy Australian preschool-aged children during a 12-month period.
http://www.ncbi.nlm.nih.gov/pubmed/22829638
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