AIDS Monkey Model Offers Promise of New Treatment

Researchers have developed a new monkey model for AIDS that has made clinical study of the disease easier, and offers the promise of new, effective treatments and vaccines in the future.

According to the study, published in the journal Science, The Rockefeller University team was able to slightly modify the virus HIV-1, responsible for most cases of AIDS, to not only infect pigtailed macaques, a species of monkey, but to cause full blown AIDS in the primates for the first time.

This specific virus to very selective, and so does not readily infect species other than its two usual hosts - humans and chimpanzees. While this may be good news for everyone else, for humans it makes studying the diseases difficult without an accurate animal model.

"HIV-1 only causes AIDS in humans and chimpanzees, but the latter are not a practical model and are no longer used for HIV/AIDS research. Our goal has been to figure out how HIV-1 could cause disease in a new host," lead author Paul Bieniasz said in a statement.

As part of the disease, human AIDS patients lose immune cells known as CD4+ T-cells. To develop a new animal model to study the disease, scientists induced AIDS from HIV-1 infection in otherwise resistant monkeys.

Although pigtailed macaques have fewer defenses against HIV-1 than most other primates due to lack of a certain protein, researchers still had to alter both the virus and the macaque immune system in order to induce AIDS.

This involved both bolstering the virus with a defense-disabling protein and weakening the monkeys' immune systems by depleting a type of white blood cell, known as a CD8 T-cell, that destroys AIDS-infected cells.

"When we depleted their CD8 cells, the infected monkeys developed disease closely mirroring that of human patients," co-author Theodora Hatziioannou explained.

"By accomplishing this with macaques, we have taken a step toward establishing a new model for AIDS that can be used universally in prevention and treatment research," Bieniasz added.