Scientists have discovered that HIV needs cholesterol, which it picks up from the first immune cells it infects, to keep the virus' outer membrane fluid. That allows it to communicate with - and disrupt - the body's immune system.
The long-term effect of this disrupted communication is to destroy the body’s normal defense against the AIDS virus, which is responsible for 1.8 million deaths each year.
But researchers say they can prevent HIV from damaging the immune system, if they remove the cholesterol from the virus’ outer membrane.
David Graham is a molecular biologist at The Johns Hopkins University in Baltimore, Maryland.
“By stealing cholesterol from the envelope of the virus, we can neutralize the subversion," said Graham. "We’ve broken the code; we can shut down the type of interference that HIV is having on the immune system.”
The cholesterol used by HIV, Graham notes, is not the same cholesterol that circulates in blood and causes coronary artery disease. He says the AIDS virus incorporates cholesterol into its membrane from plasmacytoid dendritic cells or pDCs - the first immune cells to recognize the virus. The pDC cells normally signal the adaptive part of the immune system - T cells - to form a more specific, long-lasting response.
But through its newly-acquired cholesterol membrane, Graham says HIV reprograms the immune system - starting with the first responder cells - so they become hyperactive.
“These cells are just saying, 'No way. We’re not shutting off," he said. "We are going to keep responding.' And that causes the cells of the adaptive immune system to start shutting down.”
The T-cells do not respond properly, and the virus can spread.
Graham says this might explain why scientists have so far been unsuccessful in developing an AIDS vaccine. Many candidate vaccines attempt to bolster the T-cells, which have been weakened by what the virus does to the pDC cells.
Graham, along with his colleagues at several European universities, found a way to disable HIV’s cholesterol membrane so it cannot corrupt the first-responder cells, clearing the way for T-cells to fight the HIV infection, or pathogen, more effectively.
“The immune system now treated it more like a regular pathogen that you would encounter, and we would have normal immune responses that would result in protection," said Graham.
So far, research has been conducted only in the laboratory. But Graham says he hopes studies in animals and humans will eventually lead to an AIDS vaccine.
The research, funded by Britain’s Wellcome Trust and the U.S. National Institutes of Health, is described in an article published in the journal Blood.