Researchers have determined that HIV infects cells of the brain and colon by binding with a particular co-receptor, CCR5, located on the surface of some, but not all, cells targeted by HIV.
The finding, reported by a team from the Gladstone Institute of Virology and Immunology at UC San Francisco, suggests a possible target for therapies aimed at preventing the virus's entry into these tissues and perhaps others, as well. The scientists presented their study results yesterday (February 3) at the Sixth Conference on Retroviruses and Opportunistic Infections in Chicago.
HIV-1 generally resides in the blood, infecting the immune system's T cells and, to a lesser extent, other immune system cells, increasingly compromising the body's ability to respond to opportunistic infections.
However, HIV also migrates from the blood into tissues, infecting various types of cells in the brain, colon, testes, ovaries and heart, some of which are immune system cells, some of which are not.
While these tissues are not the principle target of HIV infection, studies indicate that, when infected, cells in these tissues may be the underlying cause of some lethal HIV-associated diseases, including HIV-associated dementia and
HIV-associated cardiomyopathy, or death of heart muscle. There is also concern that cells in these tissues serve as reservoirs of latent or persistent virus that are protected from detection by the immune system, and that these hidden pools may be less susceptible to the combinations of drugs currently used to combat HIV infection, known as highly active anti-retroviral therapy, or HAART.
HIV generally initiates infection in the body by latching first onto the CD4 receptor, the loading dock on the target cell's surface, and then onto a co-receptor, normally CCR5, which is also located on the cell's surface. The multi-step binding process culminates when HIV fuses with the cell.