 By LEE BOWMAN Scripps Howard News Service March 27, 2006
But the virus does readily attach to certain types of cells deep in the lungs, both in humans and in several mammal species that have also recently been victims of the H5NI avian-influenza virus.
The findings, reported in the journals Nature and Science, help explain why even though nearly 200 people have become infected with the bird-flu virus in eight countries since 2003, mostly from close contact with infected poultry, the virus has not been easily spread from an initial human host to other people. "Our findings provide a rational explanation for why H5N1 viruses rarely infect and spread from human to human, although they can replicate efficiently in the lungs," said Yoshihiro Kawaoka, a virologist at the University of Wisconsin-Madison who led the study published in Nature. He also teaches at the University of Tokyo. The team found that only cells deep within the respiratory system have the surface molecule, or receptor, the flu virus needs to enter a cell. Flu viruses, like most viruses, need to enter and take over cells within their host to replicate and spread to still more cells. Receptors are molecules on the surface of cells that act like a lock. A virus with a complementary binding molecule - the key - can use the surface receptor to gain access to the cell, and then make infectious particles that spread to other cells. "Deep in the respiratory system, receptors for avian viruses, including H5N1, are present," Kawaoka said. "But these receptors are rare in the upper portion of the respiratory system. For the viruses to be transmitted efficiently, they have to multiply in the upper portion of the respiratory system, so that they can be transmitted by coughing and sneezing." The second study - published online by Science, carried out by a team at Erasmus Medical Center in the Netherlands - also found that avian flu attachment becomes progressively less dense in cells toward the windpipe and more dense in the cells that line the tiniest air sacs of the lungs. This probably accounts for the viral pneumonia and accompanying immune-system response surge that actually damages the lungs and shuts down oxygen exchange, contributing to the respiratory and multiple-organ failure responsible for almost all the 103 reported deaths from H5NI strains to date. The Dutch team observed a similar pattern of virus attachment in the respiratory tracts of cats and ferrets, suggesting that those animals serve as good models for human disease. Bird-flu infections have been reported in cats in Germany and Austria, and in a marten (weasel) in Germany, in recent weeks, according to the World Health Organization. The studies suggest that the bird-flu strains rapidly moving around the globe through migratory fowl and affecting millions of domestic birds in dozens of countries still have to undergo key genetic changes to spark a feared human pandemic like the one that claimed as many as 100 million people in 1918-19. And that could mean that researchers and public-health agencies have a bit more time to prepare for such an eventual shift, if it happens at all. "No one knows whether the virus will evolve into a pandemic strain, but flu viruses constantly change," Kawaoka said. "Certainly, multiple mutations need to be accumulated for H5N1 to become a pandemic strain."
On the Net:
Distributed to subscribers for publication by Scripps Howard News Service, http://www.shns.com Publish A Letter on SitNews Read Letters/Opinions
|
||
