Identifying the pathology and weaknesses of the HIV virus is problematic because of its ability to mutate and, in simplistic terms, hide in plain sight in the human body. Most research for a potential HIV vaccine has focused largely on boosting the ability of CD4+T, (T-cells), to fight the virus when introduced into the system. The occasional successes cannot be duplicated, making research of this virus a moving target that has been confounding some of the world’s best virologists for thirty years.
In the September 19 issue of the medical journal Blood, Researchers with Johns Hopkins University and The Imperial College have announced a potential breakthrough in fighting the HIV virus that causes AIDS. They have discovered a way to remove cholesterol from the cell wall, exposing it to a more effective immune response.
This cholesterol, not the same compound responsible for cardiovascular disease, is absorbed by the virus from plasmacytoid dendritic cells, (pDCs), the immune system’s first, short term, defense. This enables the virus to interfere with the signals the pDCs send to the T-cells, the secondary, long range response, creating a cascade reaction that overloads the immune system and allows the virus to proliferate. Cholesterol-inhibited virus cells are unable to manipulate the pDCs and the CD4+Ts are able to fight the weakened virus.
This research is still in the lab and has not been recreated in live test subjects, so we have a very long way to go yet before we know if this is the key to the end of the HIV/AIDS epidemic, but we can hope and pray that we’re at least one step closer.
