The H5N1 strain of influenza, also known as "avian influenza" or "bird flu," has been in the news a lot, so I'm assuming that anyone likely to read this knows more or less what it is. If you don't, there's a five-part series over on the old Aetiology site that covers things in depth (1,2,3,4,5). As new cases of this disease are identified, samples of the virus are being shipped to labs and examined in detail. Viruses are notorious for evolving rapidly, and scientists are closely following the evolution of this particular virus.
A news item in this weeks issue of the journal Nature discusses three mutations that have been found in virus samples collected from victims of the H5N1 outbreak in Turkey. At least two of these mutations, according to the article, appear to make the virus better able to attack humans. All three of these mutations involve substitutions of one amino acid for another in a protein.
Two of the mutations involve a protein that allows the virus to bind to the cells of the organism that it is attacking. The researchers don't yet know if one of them has any effect on the way the virus works. The other definitely does. It makes it easier for the virus to bind to human cells, but at a cost: it makes it harder for the virus to bind to bird cells.
The remaining mutation is found in a protein that the virus uses to copy itself. This one is quite familiar to researchers - it is one of the mutations that was found in the Spanish Flu, which appears to have been an avian influenza strain that evolved into a human strain. According to the Nature article, this change makes it easier for the virus to function in primates.
Researchers say that both of these mutations have been observed before, but these cases mark the first time that they have been found together. It's still not certain what effect they will ultimately have on the way that this virus functions, but this is definitely not a comforting discovery, even if the disease does turn out to be less fatal than feared.
The situation with H5N1 illustrates a number of things quite well. First and foremost, it illustrates the power of both molecular ecology and evolutionary approaches in studies of infectious disease. It also demonstrates the value of studying viruses in other, non-human, systems. Viruses can, have, and will evolve the ability to jump from one species of host to another. Studying viruses in other organisms can provide us with a headstart on identifying and attempting to prevent human outbreaks. Such studies could also provide us with a better understanding of the way that populations of viruses function and evolve. Finally, and most importantly, studies like these clearly indicate something that Tara Smith has been saying over at Aetiology for a while now: we badly need to invest in both our public health system as a whole, and in infectious disease research in particular.