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Tucson, Arizona
July 8, 2008
University of Arizona
researchers have sown the seeds of a virus' destruction in its
own genetic code--or rather, in the genetic code of the
organisms it seeks to infect. Their work could improve both our
understanding of how viruses work and our ability to make plants
and animals more virus-resistant.
 Working
with a virus that infects bacteria,
BIO5 member Bentley Fane
(photo), a professor in the Department of Veterinary Sciences
and Microbiology in the College of Agriculture and Life
Sciences, and James Cherwa, a graduate student in Fane's lab,
pinpointed a region of a protein that's crucial to building the
virus' structure; designed a modified version of that protein;
and then engineered the bacteria's cells to produce the modified
protein. When the virus infected cells of the bacteria, it
"recognized" the modified protein and, following the
instructions encoded in its own DNA, the virus tried to
incorporate the altered protein into copies of itself. Instead
the protein gummed up the works of the replication process,
causing the virus to "die" without producing any "offspring."
"We were shocked by just how potent the inhibitory protein was,"
Fane says. The research casts light on the biology of how
viruses work and how the proteins they create interact with one
another. It was recently highlighted in the Spotlight section of
the Journal of Virology.
We all have an interest in better understanding both how viruses
work and how to stop them from working, Fane explains. Viruses
are little more than strands of DNA or RNA surrounded by a
protein coat; they can't reproduce on their own. Instead they
invade the cells of more complex host organisms--everything from
bacteria to plants and animals--and hijack the machinery inside
those host cells in order to replicate. Along the way, viruses
can cause any number of diseases, including blights in plants
and colds, flu, and HIV in humans. Fane hopes to begin using
what he's learned to engineer virus-resistant plants. While
similar work has been done with plant viruses before, none of
those viruses had the icosahedral shape and structure Fane and
Cherwa's research focuses on.
The virus they're working with also reproduces quickly--a
generation lasts all of about 20 minutes—which means their
research provides an up-close view of evolution in action. Over
the course of 200 generations, Fane and Cherwa have watched the
virus evolve a mutant strain that can not only replicate in
spite of the inhibitory protein, but that may also—according to
some very preliminary research—be somewhat dependent on the
protein. In other words, the original strain's inhibitory
protein poison just may be the resistant strain's medicine.
That resistant strain would have a hard time surviving outside
the lab, because its resistance is pretty much the only thing it
has going for it—it is otherwise less healthy than the original
virus. "When something mutates, it does so at a cost to its
usefulness," Fane explains. "It's always illuminating to see how
a virus adapts to something like this, though, because it always
manages to. That's the power of evolution and selection." |
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