In a development in the research of AIDS came a breakthrough when Paul Bieniasz's Laboratory of Retrovilogy at Rockfeller University and Theodora Hatziioannou's laboratory at Aaron Diamond AIDS Research Center came up with a new animal model by modifying how HIV-1 virus interacts with the immune system of pigtail macaque monkeys. HIV-1 causes aids only in humans and chimpanzees.
Paul Bieniasz said, "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. The new animal model will change the course of AIDS research. Our goal has been to figure out how HIV-1 could cause disease in a new host. 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."
After years of research, a reliable animal model has been found. The researchers strengthened the virus with a defense-busting protein taken from a cousin to HIV-1, Simian Immunodeficiency virus. After the virus was allowed to stay in the infected animal's body for a while, the researchers weakened the immune system of the monkey by targetting CD8-T cells, a type of white-blood cells, that destroys virus-infected cells. Theodora Hatziioannou said "The new animal model closely mirrors the human experience with the virus. Because it replicates what happens when HIV-1 compromises a human patient's immune system, our approach could potentially be used in the development of therapies and preventative measures for human patients. When we depleted their CD8 cells, the infected monkeys developed disease closely mirroring that of human patients. Still, the new animal model is not an exact replica of the human immunological response given the need to first deplete immune cells. We still have one major hurdle to overcome: If we could get HIV-1 to cause AIDS without depleting the CD8 cells, we could replace models that make use of SIV for this research. This new model for HIV-1 infection is the result of years spent exploring scientific questions about how the virus interacts with a host's antiviral defenses. These kinds of basic insights will enable us to continue to improve this model."