The strategy of Woodruff Health Sciences Center | Feb. 24, 2016
A strategy called "kick and kill", for the activation of latent HIV-infected cells so that the virus can be destroyed, there arose a period of time ago.
Yerkes researchers have been looking for a possible way to do it in a model non-human primates (SIC) and reported their findings at the Conference on Retroviruses and Opportunistic Infections in Boston.
An immune booster treatment may force the SIV (Simian Immunodeficiency Virus) out of their hiding places in infected monkeys who have controlled the virus with antiretroviral drugs, report scientists at the National Research Center of the University of primatesEmory in Yerkes. The results were presented on Wednesday, February 24 at the Conference on Retroviruses and Opportunistic Infections in Boston for a graduate student named Geetha Mylvaganam. Rama Rao Amara, PhD, Professor of Microbiology and Immunology Yerkes and the Emory Vaccine Center, led the project. Employees involved in the study, as Rafi Ahmed, PhD, director of the Vaccine Center and a leading scholar of Emory Georgia, the European Alliance for Research and Gordon Freeman, PhD, of the Institute of the Dana-Farber Cancer. Mylvaganam is part of the graduate program in molecular pathogenesis and immunology at Emory.
With control of antiretroviral drugs can usually keep HIV in chronically infected persons, but can not eliminate it completely. This is because some immune cells harboring the virus in a latent state. A strategy has emerged called "kick and kill", for the activation of these cells so that the virus can be eliminated from the body.
The Yerkes team tested the effects of blocking Pd 1, a molecule that inhibits the immune response during chronic infections, in combination with antiretroviral therapy. Antibodies that block 1-PD have also been tested with some success in immunotherapy against cancer agents The team developed an antibody "primatized" anti-PD 1 to reduce immune responses of monkeys antibody itself and allow repeated infusions.
With some monkeys infected with SIV, the researchers treated them with anti-PD-1 14 antibody per day, beginning ten days before the initiation of antiretroviral therapy. In this situation, the animals treated with the anti-PD-1- showed a more rapid viral suppression (mean 42 days in PD-1 140 group versus controls in days) and a higher amount of active antiviral T cells.
In addition, monkeys infected with SIV were treated with anti-PD-1 antibody (three infusions, with one month between each) after antiretroviral therapy had brought viral levels to a very low level. This resulted in transitional SIV reappearances in his blood, not seen in animals used as control.
The researchers conclude: "These results show for the first time PD-1 the blocking potential, both on the restoration of antiviral T CD8 cell function, and possibly destabilize the viral reservoir on ART. They highlight the potential PD-1 lock to work synergistically with other therapeutic agents such as vaccines and latency agents to effectively reduce the HIV reservoirs in the ART as a means of establishing a functional cure ".
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