Scientists have confirmed Human Immuno-deficiency Virus (HIV) can survive in another less-explored type of white blood cell. Until now...
Scientists have confirmed Human Immuno-deficiency Virus (HIV) can
survive in another less-explored type of white blood cell. Until now,
treatment and cure research has focused on blocking the virus from
T-cells, a type of white blood cell that is key to the immune system.
However, new research by the University of North Carolina (UNC),
United States (U.S.), reveals the virus can also persist exclusively in
macrophages, large white blood cells found in the liver, lung, bone
marrow and brain.
The breakthrough discovery could explain why – despite monumental
advances in suppressing the virus – no treatment has successfully cured
anyone of the disease.
“These results are paradigm changing because they demonstrate that cells other than T cells can serve as a reservoir for HIV,” said Dr Jenna Honeycutt, lead-author and postdoctoral research associate in the UNC Division of Infectious Diseases. “The
fact that HIV-infected macrophages can persist means that any possible
therapeutic intervention to eradicate HIV might have to target two very
different types of cells.”
HIV treatments have advanced to the extent that a daily regimen of
pills can make the virus undetectable and non transmittable. Roughly 30
percent of America’s 1.2 million people with HIV have reached an
undetectable viral load.
A person with HIV becomes ‘undetectable’ when treatment
targeting T-cells suppresses the virus to a level so low in their blood
that it cannot be detected by measurements. If a person is undetectable
and stays on treatment, they cannot pass HIV on to a partner. No study
has ever shown HIV transmission from someone with an undetectable viral
load.
To date, an undetectable load is almost always achieved with daily doses of antiretroviral drugs.
But a number of clinical trials – including PRO-140 by CytoDyn,
which Charlie Sheen is involved in – hope to be developing treatments
that could be administered on a weekly or fortnightly basis.
This endeavor could be transformed by the latest UNC research,
which builds on years of speculation in the HIV research community. Last
spring, UNC School of Medicine demonstrated that tissue macrophages
supported HIV’s survival in the body, independent of human T cells.
But how macrophages would respond to antiretroviral therapy (ART)
was unknown. They also were not sure whether macrophages could be a de
facto reservoir for HIV after treatment, or whether they simply
supported the virus.
Macrophages are myeloid lineage cells that have been implicated in
HIV pathogenesis and in the trafficking of virus into the brain.
Using a humanized myeloid-only mouse (MoM) model devoid of T cells,
Garcia and his team showed that ART strongly suppresses HIV replication
in tissue macrophages.
Yet when HIV treatment was interrupted, viral rebound was observed
in one third of the animals. This is consistent with the establishment
of persistent infection in tissue macrophages.
“This is the first report demonstrating that tissue macrophages can be infected and that they respond to antiretroviral therapy,” Honeycutt said.
“In addition, we show that productively infected macrophages
can persist despite ART; and most importantly, that they can reinitiate
and sustain infection upon therapy interruption even in the absence of T
cells – the major target of HIV infection.”
Now that Garcia and his team know HIV persists in macrophages, the
next step will be to determine why and how HIV persists in tissue
macrophages.
They will also investigate where in the body persistently infected
macrophages reside during HIV treatment, and how macrophages respond to
therapeutic interventions.
-Adapted from DailyMailUK Online
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