HEALTH
Scientists Say Protein Guards Some Monkeys Against HIV
By MARILYN CHASE
Staff Reporter of THE WALL STREET JOURNAL
Scientists said they identified a protein that shields rhesus monkeys
from the AIDS virus, a finding that opens new avenues for drug and
vaccine research.
The protein, called TRIM5-alpha, is believed to be part of the innate
immune system that patrols the body looking for invaders and blocks
their ability to infect.
People make a version of TRIM5-alpha that is 87% identical to the
monkey protein, but isn't able to thwart AIDS. Scientists said they
hope to find ways to beef up that human protein or to use the monkey
protein in treatment or prevention.
Joseph Sodroski, an AIDS researcher at the Dana-Farber Cancer Institute
in Boston, and Matthew Stremlau, a Ph.
D. candidate at Harvard Medical
School, reported the discovery with co-workers on Wednesday in the
journal Nature.
Anthony S. Fauci, director of the National Institute of Allergy and
Infectious Diseases, said the finding sheds new light on the HIV life
cycle and "opens new avenues for intervening in early stage of HIV
infection before the virus can gain a toehold."
The discovery caps almost a decade of work into why the human
immunodeficiency virus (HIV) infects some animals and not others.
Scientists long had wondered why Old World monkeys -- a group including
rhesus monkeys (or macaques), baboons and mangabeys -- didn't get AIDS.
"It became clear that monkeys were making a potent and specific factor
blocking HIV," said Dr. Sodroski.
But isolating it took "heroic efforts" by Mr. Stremlau to pluck a gene
for this protective factor out of the 40,000 genes in a monkey's
genome, Dr. Sodroski said.
"I
t was like looking for a needle in a haystack," said the 27-year-old
Mr. Stremlau. First he made a library of all 40,000 genes. Next, each
gene was put into human cells normally vulnerable to infection by HIV.
Then they unleashed HIV to observe the effect of the genes on
infection.
To screen cells that got infected from those that didn't, the team had
engineered HIV to emit a green fluorescent light to signal when
infection occurred. Infected cell cultures shone bright green; a dark
culture signaled infection failed. One stood out as especially well
protected.
"Cells carrying the gene for TRIM5-alpha didn't get infected, no matter
how much HIV you put on them. They remained dark," said Dr. Sodroski.
"It is really potent in blocking HIV."
Making the discovery was "like winning the lottery," said Mr. Stremlau,
who was drawn to AIDS research after family travels in Africa.
Dr. Sodroski said questions still
remain as to how the protein works,
and whether variants exist in humans that may protect some people from
getting AIDS. Among future possibilities, he said, the protein could
lead to gene therapy, to vaccines, to improved animal models, or
eventually to drugs that mimic the most active part of the protein.
The work was funded by grants from the National Institute of Allergy
and Infectious Diseases, the International AIDS Vaccine Initiative, the
Bristol-Myers Squibb Foundation, and the Center for AIDS Research of
Dana-Farber, Beth Israel Deaconess Medical Center and Children's
Hospital Boston.
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