For many viruses, infiltrating cell replication and is only half the battle. Copies of the virus must then escape to infect other cells. Some viruses explode outside a host cell, destroy; others, like the influenza virus, taking a softer way. Now, a report in the latest EMBO Journal shows how the flu virus slips the bounds of his cell -. Prisoner and how, by knocking out parts of two key viral genes, it can be held
After the influenza virus invades a cell, it commandeers the cell genetic mechanism to multiply the viral RNA. The viral proteins assemble new virus particles that migrate to the cell wall, where they wrap themselves in the membrane. The bud, as it is called, clamp off and escapes. "It's almost like bubbles," said Robert Lamb, a virologist at Northwestern University.
The virus escape tools were thought to be two proteins, hemagglutinin and neuraminidase, which jab like grappling hooks in the cell membrane, leaving "tails" dangling for viral particles to enter on to test the importance of these protein "spike" to Houdini act of the virus, Lamb and his colleagues performed a simple experiment.: they disabled one, then two, portions of genes from influenza viruses encoding the tail proteins. viruses can manufacture one full spike protein had a time a little harder bud formation in cultured cells. But the effect on viruses without two tails protein was superb. the number of viral particles escaping from each cell has dropped by 0%, and the escapees were severely deformed instead of balloons, Lamb said, they looked like a "sausage chain with big bulges coming out the side -. As something of science fiction "
The deformed virus, not surprisingly, had a much harder time to infect new cells that made their spherical brothers. This could make the tails of a protein spikes tempting target for new drugs, says virologist John Rose of the medical School of Yale University, who called the research "an important work."
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