This article is reposted from the old Wordpress incarnation of Not Exactly Rocket Science.
It's not just us who like to go travelling in the summer - flu viruses do it too. After a busy winter of infection, they turn into the gap-year students of the virus world. They travel round the world, meet new viruses, swap genetic material, and returning back, changed and unrecognisable (at least to our immune systems).
The success of flu viruses hinges on their ability to rapidly fool our immune systems by changing the proteins that line their surface. Every year, they put on a new disguise that shield them from any immunity built up the year before, allowing them to constantly re-infect the same populations of people.
But when scientists looked for these fast evolutionary changes during the epidemic season (November to March in the northern hemisphere), they found surprisingly little. That suggests that the viruses evolve their new facades during their off-season and it could do so in two ways.
They could stay within the same host population in a dormant state, until changing climate stirs them into action. Alternatively, they could travel to other parts of the world, only to return the following year.
One of the problems with deciding between these theories is a lack of data. The World Health Organisation has an excellent network of influenza reference centres but for obvious reasons, they don't keep an eye on the viruses outside of the epidemic season.
But Martha Nelson and colleagues form Pennsylvania State University and the National Institutes for Health realised that they didn't actually need this data. They compared the genomes of virus samples collected during several epidemic seasons in America, Australia and New Zealand.
If they stayed in the same place, then viruses collected in different years at the same place would be genetically closer than viruses collected elsewhere. However, if the viruses travelled between busy seasons, their evolutionary relationships would be much more mixed, with some northern viruses being more closely related to southern viruses than their neighbours.
That's exactly what Nelson found after sequencing the genomes of over 900 samples of the H3N2 influenza A virus. When she built an evolutionary tree of her samples, she saw clear signs of significant viral traffic across the equator in both directions.
In fact, she found no examples at all where viruses from the same place were genetically closely linked across different seasons. Even viruses from relatively isolated countries like Australia and New Zealand travelled and evolved elsewhere.
So during the off-season, flu viruses travel to foreign lands where they change their genetic make-up. Nelson's study doesn't tell us where this happens, but she thinks that the tropics are the best bet.
In the tropics, influenza is a year-round problem. Nelson believes that the tropical belt acts like a virus training camp. Every year, it receives recruits from temperate areas that have been recognised by the immune system, fits them with new mutations, and chucks them back out to start new epidemics. An increase in air travel could certainly be aiding the viruses in their journeys.
South-east Asia in particular could be a genetic melting pot for flu viruses because of the large populations there who live in close contact with their domestic animals. Of course, all of this is just an educated guess until the team can get their hands on some tropical flu samples.
Nelson also wants to find out why flu viruses in temperate zones take the summer off, when they happily infect all year round in the tropics. What climate-related cues quell the epidemics?
Again, she stresses that we'll only get these answers by collecting more samples, throughout the year and in various parts of the world. That would be a vital step toward understanding the hidden life cycle of flu viruses, and how these can be disrupted.
Reference: Nelson, Simonson, Vibound, Miller & Holmes. 2007. Phylogenetic analysis reveals the global migration of seasonal influenza A viruses. PLoS Pathogens 3: e131.
