This is a huge step closer to eliminating the HIV virus. We know the
key protein and we know that we have to turn it of to win. This is
at least a clear pathway.
The disease itself is now well controlled but certainly not cured.
Eliminating these reservoirs opens the door to an outright cure.
This will ultimately be described as one of the greatest battles in
medical science but also one of the most productive in terms of new
science.
I do think that we are in the homestretch with HIV. This is not the
only route now.
Discovery may help
prevent HIV 'reservoirs' from forming
by Staff Writers
Bronx NY (SPX) Apr 19, 2013
Researchers at Albert
Einstein College of Medicine of Yeshiva University have discovered
how the protein that blocks HIV-1 from multiplying in white blood
cells is regulated.
HIV-1 is the virus
that causes AIDS, and the discovery could lead to novel approaches
for addressing HIV-1 "in hiding" - namely eliminating
reservoirs of HIV-1 that persist in patients undergoing
antiretroviral therapy. The study was published in the online
edition of the journal Cell Host and Microbe.
Antiretroviral therapy
can reduce blood levels of HIV-1 until they are undetectable. But
despite drug therapy, reservoirs of HIV-1 can persist in several
types of white cells, notably macrophages - important immune cells
that help clear pathogens and other potentially harmful substances
from the body.
"If you stop
antiretroviral therapy, the virus emerges from these reservoirs and
returns to the general circulation in a matter of days, as if the
patient had never been treated," said senior author Felipe
Diaz-Griffero, Ph.D., assistant professor of microbiology and
immunology at Einstein. "Now we know the protein that we need
to control so we can prevent HIV-1 reservoirs from forming or
eliminate them entirely."
Scientists have known
that a protein called SAMHD1 prevents HIV-1 from replicating in
certain immune cells. But until now, it was not understood why SAMHD1
fails to function in immune cells like macrophages that are
vulnerable to HIV-1 infection.
Using mass
spectrometry, a tool for determining molecular composition, Dr.
Diaz-Griffero found that SAMHD1 can exist in two configurations known
as phosphorylated and unphosphorylated. (Phosphorylation is an
important cellular process in which phosphate groups attach to other
molecules, thereby activating various signaling and regulatory
mechanisms within the cell.)
When SAMHD1 is
phosphorylated - the situation in immune cells that divide - the cell
is not protected from being infected with HIV-1. When the protein
is not phosphorylated - as occurs in the nondividing macrophages
- the cell is protected from HIV infection.
"We are currently
exploring ways to keep this protein unphosphorylated so that HIV
reservoirs will never be formed," said Dr. Diaz-Griffero.
The title of the paper
is "The Retroviral Restriction ability of SAMHD1 is Regulated by
Phosphorylation." Other Einstein contributors are Tommy E.
White; Alberto Brandariz-Nunez, Ph.D.; Jose Carlos Valle-Casuso,
Ph.D.; and Marina Tuzova. Additional authors include Sarah Amie,
Ph.D.; Laura Nguyen, Ph.D.; and Baek Kim, Ph.D., all at the
University of Rochester School of Medicine and Dentistry, Rochester,
NY. The study was funded by a grant (AI087390) from the National
Institute of Allergy and Infectious Diseases, part of the National
Institutes of Health.
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