Thin Line Stops Bird Flu Spread
Bird Flu Can't Infect Human Nose or Throat -- Yet
WebMD News Archive
March 22, 2006 - A thin red line now keeps people infected with bird flu from infecting others.
This shallow line of defense is a matter of anatomy -- at the cellular level. A new study shows that bird flu can infect cells that line the human lung. But it can't infect most of the cells lining the nose, throat, and sinuses.
Getting the bird flu virus deep in the lung is hard to do, but it can be lethal when it happens. However, spreading the virus is another story. If the virus can't replicate in the nose and throat, it can't be spread by sneezing and coughing.
This may explain why the sparks that could set off a bird flu pandemic -- to date, 184 human infections with the deadly H5N1 strain of bird flu -- have never turned into a conflagration, says study leader Yoshihiro Kawaoka, DVM, PhD. Kawaoka is professor of virology at the University of Wisconsin, Madison.
"It has been an enigma why people get sick and die from H5N1 avian flu virus, but the virus does not spread well in humans," he tells WebMD. "Our finding explains it."
Kawaoka's research team reports the findings in the March 23 issue of the journal Nature.
How Flu Virus Hooks Up
What stops the bird flu? Viruses infect cells by latching on to receptor molecules on the cell surface. Flu viruses bind to sialic acid (SA) receptors.
Most H5N1 viruses -- there are now many strains -- need a receptor in the alpha2,3Gal configuration. In humans, only deep lung cells carry that SA configuration. Nose, throat, and sinus cells have SA in the alpha2,6Gal configuration.
If that doesn't sound very different, it isn't. It would only take a few small mutations for the bird flu virus to be able to latch on to human cells, Kawaoka says.
Flu expert David Topham, PhD, of the University of Rochester, N.Y., says this part of the flu virus mutates rapidly.
"It is relatively easy for the bird flu virus to accommodate such a thing," Topham tells WebMD. "And when people get the infection deep in the lung, there would be selective pressure on the virus to acquire this mutation. So this adaptation to humans might not have to happen in another species. It might occur in humans."
In fact, it's already happened. Kawaoka finds that an H5N1 virus isolated from an infected patient in Hong Kong already was able to hook up to SA receptors throughout the human respiratory system. The world may have dodged a bullet when that virus failed to spread.
Kawaoka says bird flu viruses have to collect other mutations, in addition to the SA-receptor mutation, in order to cause a human pandemic.
"One mutation that makes the avian virus grow better in human cells was found in recent human H5N1 viruses -- which was scary," he says. "We don't know how many mutations in different genes are required for the avian influenza virus to become a human pandemic. That is the problem. We don't know where we are."