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HIV reputedly causes a chronic infection that can
fester for years before it manifests itself in the form of AIDS-related
symptoms. But according to Dr. Ashley T. Haase — a leading
investigator in the pathogenesis of HIV and other slow-progressing
retroviruses called lentiviruses — this perception belies
an intensely fast-paced series of events that take place during
the first few weeks following transmission. These events — including
a brief window during which the virus is at its most vulnerable — will
be the focus of his discussion as he gives the NIAID James C. Hill
Memorial Lecture on Thursday, May 26, at 2 p.m. in Lipsett Amphitheater,
Bldg. 10. The lecture is titled "The Critically Important Fast
Phase of the Slow Infections Caused by Immunodeficiency Viruses."
Continued...
"With HIV and its close relative in monkeys, simian
immunodeficiency virus, so many really interesting developments happen
immediately after transmission," says Haase, a Regents' professor
and head of the department of microbiology at the University of Minnesota. "In
order to better understand the virus and its ability to outmaneuver
the body's immune system, we need to examine
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Dr. Ashley T. Haase of the University
of Minnesota will give the Hill Lecture on May 26 in Lipsett. |
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the processes that are unfolding over the first few weeks." system,
we need to examine the processes that are unfolding over the first
few weeks."
Haase will describe key events that occur in female monkeys immediately
after simian immunodeficiency virus (SIV) crosses the vagina's
mucosal barrier — the protective lining of the respiratory,
reproductive and gastrointestinal tracts that helps the body fight
off disease-causing microbes. He'll delve into the changes that
occur with memory helper T cells — immune cells that the
body produces to help fight a subsequent infection, and the very
cells that SIV, and HIV, preferentially first infect because of
their availability. According to Haase, the virus hijacks memory
helper T cells so that it can make copies of itself while catching
a ride to the lymph nodes and lymph organs, enabling the virus
to spread throughout the body. At the same time, it triggers the
large-scale destruction of memory T cells in the gut, one of the
largest reservoirs of infection-fighting cells. As the virus multiplies
and immune cells plummet, the virus quickly overpowers the body's
ability to fight it.
For these reasons, Haase suggests that the critical time to attack
HIV is within the first few days of transmission, when the virus
is at its lowest numbers after having passed through the mucosal
barrier.
"The mucosal barrier does an effective job at keeping the virus out, and very few viral particles
make it across," he says. For him, the most promising means of HIV prevention would be an HIV-killing
gel that can bolster the effectiveness of the mucosal barrier, allowing even fewer viral particles
through, or a robust vaccine that can quickly build up the numbers of HIV-destroying killer
T cells at the mucosal surface.
Haase's work on the prototypic lentivirus in sheep, called visna,
has been awarded the Sen. Jacob Javits Award in Neurosciences from
the National Institute of Neurological Disorders and Stroke. He
is also a two-time recipient of NIH's MERIT (Method to Extend Research
in Time) Award for his work on HIV and SIV, and is a member of
the National Academy of Sciences' Institute of Medicine and American
Academy of Microbiology.
The lecture is dedicated to the memory of Dr. James C. Hill who,
as former NIAID deputy director, helped build the institute's HIV/AIDS
research program during the early years of the epidemic.
A reception outside of Lipsett Amphitheater will be held following
the lecture. 
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