Viruses can move: tale of a telltale tail.

Viruses are nature's great hijackers. They take over a host cell's biochemical machinery to make their own proteins as well as new genetic material. Now, scientists report that when viruses are poised to infect something new, they sometimes also make use of protein filaments from the host to help them move from one cell to the next.

In the Dec. 7 Nature, a research team led by Michael Way of the European Molecular Biology Laboratory in Heidelberg, Germany, describes electron microscope studies of vaccinia viruses in laboratory-grown human cells. Vaccinia viruses cause cowpox and are the source of the word "vaccine" because they are the basis of smallpox vaccines.

In the micrographs, vaccinia viruses appear to push through the surfaces of cells, propelled by long tails of actin, a protein normally part of the cell's internal skeleton. The viruses assemble these tails from intracellular actin filaments. When the researchers add agents to block assembly of the filaments, the viruses lose their tails and don't exit cell membranes.

The technique may not be exclusive to viruses.

"Similarities between what happens in vaccina and in some bacteria," Way says, "make us think they may use a basically common mechanism." Scientists already knew that actin tails propel the intestinal disease bacteria Shigella and Listeria. In the July 3 Proceedings of the National Academy of Sciences, Julie A. Theriot of the Massachusetts Institute of Technology and Marcia Goldberg of Albert Einstein College of Medicine in New York described the role of a protein that bacteria use to turn on their actin motors.

Although researchers have not identified a comparable protein in vaccinia, Way says, the mechanism is likely to be similar in the two types of microbes because both viruses and bacteria amble through cells at 2.8 micrometers per minute, even though the virus is far smaller than the bacterium.

Vaccinia viruses spread either by rupturing the host cell and escaping or by exiting the cell without destroying it, says Way. The actin tails may explain the second route, he says.

Like vaccinia, the AIDS virus also exits without rupturing the host cell, says Theriot, who believes Way's work may prompt researchers to see if actin filaments play a role in AIDS virus release.