Media Release: 22 September 2009
Australian scientists discover a major new reservoir of HIV in the brain
Scientists have discovered that infection of a particular brain cell type called astrocytes is extensive in patients with
human immunodeficiency virus (HIV)-associated dementia. Prior to the publication of this finding in the August
edition of the prestigious scientific journal, Annals of Neurology, astrocyte infection with HIV was considered rare,
so astrocytes were thought to play a minor role in the development of this disease.
The findings were the result of collaborative research led by the Burnet Institutes Dr Melissa Churchill and
involving scientists from the Burnet Institute and Monash University in Melbourne, St Vincents Hospital in Sydney
and John Hopkins University in Baltimore, USA.
HIV-associated dementia is caused by infection of the central nervous system with HIV, and is a debilitating
complication in people living with HIV/AIDS. It is, in fact, the most common cause of dementia in people under the
age of 40, and places considerable pressure on health resources in Australia and around the world. HIV-associated
dementia usually occurs at the later stages of HIV infection, when the immune system of patients is failing, but in
some people it can occur rapidly, within a few years of contracting the virus.
Even though there are excellent drugs to treat HIV infection, doctors are seeing more patients with HIV-associated
dementia. This is thought to be for two reasons; firstly fewer patients are now dying from AIDS before the onset of
HIV-associated dementia, and secondly because most currently available drugs are inadequate for treating brain
infection because they penetrate the brain poorly.
Astrocytes are the most abundant cell type in the brain. They have many important functions that are critical for
normal functioning of the brain. One major function is to maintain an optimal environment for neurons, which are
the brain cells that instruct the body how to function. It is possible that in HIV-associated dementia, astrocytes may
stop functioning normally when they are infected with HIV, which may then result in neurons dying or not
functioning normally. Unlike other cell types in the body such as certain white blood cells of the immune system
which constantly regenerate, astrocytes are long-lived and do not readily regenerate. Therefore, the effect that HIV
has on astrocytes may be long-term or even permanent.
There is presently a major focus in the field of HIV research to identify novel ways to permanently eradicate HIV
from the body (effectively curing HIV infection), in particular from so-called viral reservoirs that are hard to treat
with anti-HIV drugs. The results of this new study highlight the brain as an important viral reservoir. Therefore, the
new strategies that are being designed to eradicate HIV from the body must also be designed to eradicate virus
from brain astrocytes, in order for HIV infection to be completely cured.
Co-author of the article, and current Dean of Medicine at Monash University, Professor Steve Wesselingh said,
The results of this research are extremely important to HIV research and the HIV community as it gives greater
insight into HIV-associated dementia, and although HIV-associated Dementia has a more rapid onset then age-
related dementia or Alzheimers and is caused by a virus, this research is also highly significant in understanding
Alzheimers.
Professor Bruce Brew, Head of Neurology at St Vincents Hospital in Sydney said This is a very significant step
forward as it identifies a significant viral reservoir with direct implications for eradication therapies. Furthermore, it is
potentially another explanation for the continuing presence of cognitive impairment in antiviral treated patients as
the efficacy of current antiviral drugs in astrocyte infection is limited at best.
Co-author and Head of Neurology at Johns Hopkins University in Baltimore, Professor Justin McArthur said, HIV-
associated neurological disorders remain prevalent despite the widespread use of highly active antiretroviral
therapy. There appears to be a therapeutic gap between the salutary effects of antiretroviral regimens and
normalisation of neurological function. A second gap is in the understanding of the pathology and pathophysiology
of HAND. This work provides a new insight into the pathophysiology of HIV infection within the brain, and may lead
to new therapeutic targets to bridge this gap.
More Information
Media Enquiries:
Tracy Routledge,
Senior Public Affairs Officer, Burnet Institute
PH: 61 3 9282 2240 or 61 (0) 0412 223 221
E: tracy@burnet.edu.au