If you’ve paid any attention at all to the news during the past several months, chances are you’ve heard about the controversial studies being conducted on the H5N1 virus, otherwise known as the bird flu. Then again, even if you have been paying attention to the news, with all the feces being smeared across the media landscape in honor of the Republican Presidential Primary, perhaps you haven’t.
Two separate researchers – Yoshihiro Kawaoka from the University of Wisconsin and Ron Fouchier of Erasmus Medical Center in Rotterdam, The Netherlands – were tinkering around with the genetics of the deadly flu in their labs. The idea – create a ton of random mutations and see which, if any, give the flu strain the ability to easily spread through mammal populations.
Sounds a bit like “I Am Legend,” no? Some scientists in a lab working to create an even more deadly strain of an already problematic virus. What if it accidentally got out of the lab? What if bioterrorists took the information from the study to create their own weapons?
When word about the studies got out, people had a conniption fit.
So the scientists agreed to put their research on a 60-day hiatus in order for the general scientific community to hash out whether or not the details of the studies should be released, and indeed, if the experiments should even be taking place.
Well, after the fit was over, those involved agreed that the science was important enough to take the risks – real or perceived – and publish the paper. Kawaoka’s came out in Nature just this week.
Here’s what it says.
Kawaoka created millions of strains of the H5N1 virus, each with its own tiny little mutation. The hope was that one would allow the virus to be able to jump between mammals more easily. In this way, he hoped to gain insight into what mutations might cause the virus to do the exact same thing out in the natural world. By understanding what to look out for – he argued – we would be better prepared to fight off a plague of H5N1, should it ever come to that in the natural world.
Well, he succeeded. Just one of those strains proved to be able to infect ferrets, the animal model used to represent a human’s immune system. Bird cells have slightly different receptor proteins on their surface than humans. Since the H5N1 virus needs to stick to these receptor proteins in order to infect the cell and it is designed to stick to a bird’s, it doesn’t stick to a human’s well at all.
But that one strain created by Kawaoka had just two mutations that allowed it to to stick to the human-like receptors found in ferrets.
Next, he fused seven genes from the swine flu to the newly created strain, in order to try to get the virus to be able to spread between ferrets. This sort of genetic swap happens all the time in nature between viruses, bacteria and all sorts of creatures, so it’s really not a far-fetched idea.
Two generations of viruses later, the new strain of bird flu was able to infect 100% of the ferrets exposed to it. This is a huge leap from barely being able to infect any at all. But this time, it wasn’t Kawaoka’s doing.
It was nature’s.
When Kawaoka looked at the DNA of the highly virulent virus, he discovered that it had picked up two additional mutations through evolution that allowed it to spread so easily. And making that big of a jump so quickly is quite an impressive feat.
All of these details – and the exact mutations picked up by the virus – are now in the public domain. Anybody can read about the procedures Kawaoka took to create the virus.
So what does that mean?
Well, first of all, the chances of any bioterrorist out there having the knowhow and equipment to pull something like this off is just a pubic hair above completely impossible. And while accidently releasing the strain through the biolabs is a real concern, the precautions being taken are pretty strong.
Of course, the chances of the bird flu naturally acquiring all of these exact mutations in nature is also just about zero. But that’s not the point. The point is that there are countless other combinations of mutations that could happen that would allow the virus to spread through the human population like wildfire, and studies like these give us a clue as to what to look for.
Three of the mutations allowed the virus to stick to the protein receptors in ferrets. But the fourth one stabilized the stalk of the virus. Before that fourth mutation, the other mutations caused the virus to unleash its DNA on the cell before it was actually inside of it.
The three mutations caused it to become a premature ejaculator.
But that fourth one, again, stabilized it so that it infected the cell at just the right time again. This type of mutation wasn’t even on Kawaoka’s radar before the study. Nobody had thought that this type of a mutation is what would be the difference between being easily transmissible and not.
Thus, studies like these give viruologists out in the field an idea of what to look for. If natural viruses out there begin to take on mutations that cause similar changes – or other changes yet to be identified as important – they might be able to identify the threat.
So while there are dangers involved in these studies, they’re probably worth the risk. And besides, the new mutant strains created in Wisconsin didn’t even kill a single ferret.