Burnet research identifies new way of fighting HIV

Burnet Institute

07 December, 2012

Dr Clovis Palmer in the laboratory.

This article appeared in the Star Observer, written by Benn Dorrington.

In a world first, a Melbourne researcher has proven HIV not only affects the function of immune cells in humans but affects how these cells metabolise energy.

The finding could lead to new drugs that delay the start of anti-retroviral therapy and strengthen immune systems for some HIV-positive people at a higher risk of life-threatening diseases.

Dr Clovis Palmer from the Burnet Institute began his study last year after he was offered a Creative and Novel Ideas in HIV Research grant to understand how HIV affected cell metabolism in immune cells.

Palmer said CD4 T cells failed to adequately replenish themselves in up to 30 percent of HIV-positive individuals after taking long term anti-retroviral therapy and have undetectable viral load.

CD4 T cells are a type of white blood cell which help fight infection and disease in the human body, however HIV attaches itself to these cells and attacks them, damaging the immune system and leaving people prone to other infections.

Healthy adults have between 600 to 1,200 CD4 cells in their blood but up to 30 percent of HIV infected adults have a CD4 cell count consistently less than 350, well below the normal range despite undetectable viral load.These low levels of CD4 cells put HIV-positive people at higher risk of cardiovascular disease, liver disease, kidney failure and other life-threatening diseases.

For HIV-positive people with consistently low CD4 cell numbers, Palmer found CD4 T cells had high metabolic activity and produced high levels of a particular protein called Glut1.

“What we found really interesting was that this type of metabolic activity of CD4 cells was significantly associated with low CD4 count,” Palmer told the Star Observer.

“In other words, the higher the metabolic activity of these CD4 cells, the lower the CD4 count.

“The basic premise now is to find an unconventional approach to normalise the metabolic activity of these cells to bring them back to normal.

“What’s exciting about this is there is a real scenario where that by returning metabolic activity to normal, these cells could be re-energised to fight the infection by itself.”

Palmer said he believed the CD4 cells could not replenish themselves because the cells exhausted their energy reserves through the high metabolic activity.

Current HIV treatments target the virus however Palmer said this unconventional approach could lead to new treatments which targeted the actual cells and stabilised metabolic levels.

Palmer acknowledged co-investigator Burnet Institute’s Professor Suzanne Crowe and California University’s Professor Joseph McCune.

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