July 25, 2001
Contact: Tim Stephens (831) 459-2495; email@example.com
RESEARCHERS UNCOVER HOW A POX VIRUS FOOLS THE IMMUNE SYSTEM
For Immediate Release
SANTA CRUZ, CA--Research on a rabbit pox virus has shed light on how some viruses
sneak past our immune defenses. Scientists at the University of California, Santa
Cruz, have found three separate mechanisms by which the pox virus, myxoma, silences
the messengers that would normally alert the immune system when a cell is infected.
Some of these techniques are also used by herpes viruses and by HIV, the virus that
Most viruses betray themselves to the immune system by their own activities within
an infected cell. Viruses cannot replicate on their own, but use the cells they invade
as factories to reproduce themselves. Hijacked cellular machinery replicates the
virus's genetic material and builds viral proteins.
But these viral proteins tip off the host organism's immune system that something
is wrong. Specialized molecules in the infected host cells, called major histocompatibility
complex (MHC) molecules, carry pieces of the viral proteins to the cell surface,
where the immune system's T-cells recognize the proteins as foreign and kill the
One class of viruses, called DNA viruses, has evolved special genes to block the
action of the MHC molecules.
"In streamlined viruses, most genes are for virus reproduction," said Martha
Zuniga, an associate professor of molecular, cell and developmental biology at UCSC
who directed the research. "But in DNA viruses, much of the genome is devoted
to evading the host immune system."
In the myxoma research, Zuniga and her coworkers found that during the early stages
of an infection, the viral DNA produces proteins that pull MHC molecules on the cell
surface back inside the cell, where they disintegrate. As the infection progresses,
the virus also manages to hold new MHC molecules prisoner within the organelle that
makes them. And in the late stages of infection, the virus prevents fragments of
its proteins from attaching to transporter molecules that would ordinarily carry
protein pieces to the MHC molecules.
"It's as if it is covering all its bases for preventing MHC molecules from making
it to the cell surface," Zuniga said. She has summarized several years of her
research on myxoma in a review article published this month in Recent Research
Developments in Virology.
Understanding how viruses slip past immune defenses may help researchers learn
how to "tweak the system" to control viral infections, Zuniga said.
"A treatment is much more likely to work if we know all the tricks a virus has
up its sleeve," she said.
Myxoma doesn't infect humans, but it shares its evasion techniques with several viruses
harmful to humans. HIV also causes MHC molecules on the cell surface to be drawn
inside the cell. Adenovirus, a virus that causes respiratory illness, retains MHC
molecules in the cellular compartment where they are made. And herpes viruses block
pieces of viral protein from being carried to the MHC molecules.
But although these viruses produce similar effects, the causes appear to be different.
A close examination of myxoma's DNA has revealed that the genes that regulate myxoma's
evasion mechanisms are different from those of HIV, adenovirus, and herpes, suggesting
that the viruses did not all inherit the same evasion genes from a common ancestor.
"They seem to have evolved separately," Zuniga said.
Observing myxoma's evasions teaches researchers as much about MHC as about myxoma,
"A lot of what we know about MHC comes from viruses," she said. "You
can learn a lot about how something works by seeing how it gets broken."
A better understanding of MHC transport might allow scientists to block MHC in the
rare situations when its activity is harmful instead of helpful. When a patient receives
an organ transplant, for instance, the grafted organ's MHC molecules are among the
factors that prompt the body to reject the organ as a foreign object.
"If we could selectively manipulate MHC expression, we could turn it on and
off at will," Zuniga said.
Editor's note: Reporters may contact Zuniga at (831) 459-3180 or firstname.lastname@example.org.
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