Scientists say they have found a way to disarm the AIDS virus in research that could lead to a vaccine. Researchers have discovered that if they eliminate a cholesterol membrane surrounding the virus, HIV cannot disrupt communication among disease-fighting cells and the immune system returns to normal.

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.

Researchers at the Spanish Superior Scientific Research Council (CSIC) have successfully completed Phase I human clinical trials of a HIV vaccine that came out with top marks after 90% of volunteers developed an immunological response against the virus. The MVA-B vaccine draws on the natural capabilities of the human immune system and "has proven to be as powerful as any other vaccine currently being studied, or even more", says Mariano Esteban, head researcher from CSIC's National Biotech Centre.


The MVA-B vaccine first showed promising signs back in 2008 when clinical trials involving mice and macaque monkeys demonstrated a very high efficiency against Simian immunodeficiency virus (SIV). The recent human trials involved 30 healthy volunteers, where 24 were treated with MVA-B, while the other 6 were treated with a placebo, carried out over a 48 week period.

Development of MVA-B is based on the insertion of four HIV genes in a previously used vaccine (MVA) for smallpox. When injected with the vaccine, a healthy immune system can react against the MVA, whilst the HIV genes are incapable of self-replicating. This guarantees a safe clinical trial for HIV free volunteers. Furthermore by trialing the vaccine on healthy patients, the immune system can learn how to detect and combat the HIV virus components. "It is like showing a picture of the HIV so that it is able to recognize it if it sees it again in the future", says Esteban.

"Our body is full of lymphocytes, each of them programmed to fight against a different pathogen" continued Esteban. "Training is needed when it involves a pathogen, like the HIV one, which cannot be naturally defeated".


The trial demonstrated how the vaccine stimulates the production of lymphocytes B, which produces HIV attacking antibodies that block the virus from infecting healthy cells. Blood tests during the 48th week revealed that 72.7% of the treated volunteers had developed these HIV fighting antibodies. However generating a long lasting response against future attacks truly renders the vaccine effective. This is achieved when the body maintains a basic memory level of T lymphocytes, which are generated after the first attack and can circulate the body for years. The T lymphocytes are responsible for stimulating the attacked cell's immune response, which can then identify and destroy the HIV virus. Blood tests during the 48th week revealed that the 85% of the patients maintained the memory T lymphocytes immune response.

"MVA-B immune profile meets, initially, the requirements for a promising HIV vaccine," says Esteban. Although it does not remove the virus from the body, the immune response induced by the vaccine could keep the virus under control by destroying the infected cell.

According to CSIC, "if this genetic cocktail passes Phase II and Phase III future clinic trials, and makes it into production, in the future HIV could be compared to herpes virus nowadays".

Phase I clinic trials will also commence with HIV infected volunteers to test its efficiency as a therapeutic vaccine.

Source: Spanish Superior Scientific Research Council (Spanish).