By CP Staff
By Olivia LaVecchia
By Chris Parker
By Jesse Marx
By John Baichtal
By Olivia LaVecchia
By Jesse Marx
By Olivia LaVecchia
They combined to make a third, dumbed-down virus that caused mild pandemics.
The 1918 virus jumped right from birds to people. There was no combining with other viruses. One of the problems we've had is, if you look at the 1918 virus and this one, they're in essence kissing cousins. Genetically, these things look very similar. Frank Obenauer and colleagues just published a paper the last week of January in Science, and they actually have gone back and looked at the full genetic codes for 169 avian virus genomes, dating way back. They looked at 2,169 distinct avian virus genes. There were two viruses that showed a protein tag at the end of one of the nonstructural genes that actually looks to help cause the cytokine storm that makes this a unique illness.* And guess which two viruses they were: 1918 H1N1, and the current H5N1.
Then, when you look at the Turkey virus—that thing mutated. This is the case of the young girl in Turkey who died from her infection, and so did her uncle. We definitely have clusters where it's not just bird contact [spreading the virus]. The uncle's only exposure to this virus was riding in the ambulance with her from hospital one to hospital two. He became ill three days later and died. Her virus has now been fully sequenced, and there were three mutations that occurred in that virus, between the bird version and hers. One was the substitution of a glutamic acid with lysine at the 223-hemagglutinin position. That is what changes it from a bird-receptor virus to a human-receptor virus. The second thing was two other substitutions that served to make it look more and more like a human virus.
So this thing just continues to march. Changes are occurring in it all the time. [Human-to-human transmission] could happen tonight. Or it may never happen. But I don't know what will keep it from happening, because when you have this kind of worldwide bird population as we do now—China's a good example. In 1969, during the last pandemic, China only had about 12 million chickens. Now it's got over 15 billion.
CP: Do you think the rise of poultry farms of vast scale has contributed to the viral soup that influenza viruses grow in?
Osterholm: Not really, and I'll tell you why. When you look at the rise of the really big bird operations, they are actually raised in these bio-security barns, which people have all kinds of problems with for entirely different reasons—humaneness and that kind of thing. They actually are very safe, generally speaking, because they keep the wild birds and the domestic birds separate. It's in Asia where you have all these small 20-, 40-, 50-chicken operations where the birds are living in open space with you—that's where the vast majority of the chicken population is at in the developing world. A good example is Turkey, where we're seeing the first cases outside of Asia now. This is taking the virus out of a tropical area and putting it in a temperate area that gets cold. Every night, those people bring their chickens into the house. It's just a very different mindset.
And for as much as this is going to come here someday, [bird-to-human transmission] is not going to be a big risk factor to humans on this continent, because other than free-ranging organic birds that are out there, domestic birds aren't going to be at big risk.
CP: Can you explain in lay terms what makes a strain like H5N1 novel, and so potentially deadly?
Osterholm: Well, there are three things that make a strain of influenza virus potentially capable of causing a pandemic. First of all, you have to have a situation where you've got a novel or a new strain, meaning you don't have any antibody protection against it. Then you have to have one that is able to go from human to human. That's what we don't have yet. The third thing is, it has some virulence characteristics that make it cause severe illness.
This virus is quite different from what we see with the standard annual flu, and what we saw in 1957 and 1968, because of the cytokine storm it causes. In 1918, the vast majority of the people who died were healthy young people, 20 to 40 years of age. And that was in large part because they had the strongest immune systems.
CP: You're saying that the symptoms that cause fatalities, aside from secondary bacterial infections, are actually a function of the immune system working overtime.
Osterholm: That's it. And that's what we're trying to understand at this point, in terms of how to best prevent this [immune reaction]. And right now it doesn't look like there's much you can do. I mentioned this "kissing cousins" phenomenon. If you put 1918 H1N1 into animal models at very, very low doses, it basically kills all of them in 24 hours. The lab science people had never seen that. At 16 to 24 hours, that virus was different from anything they'd ever seen in killing these animals. The only virus that was similar was H5N1, and it was fatal at much lower doses. H5N1 is the most powerful influenza virus we've seen in modern human history.