THC Mitigates HIV

Philadelphia, PA: The administration of synthetic cannabinoid agonists limits HIV infection in macrophages (white blood cells that aid in the body's immune response), according to preclinical data published in the Journal of Leukocyte Biology. Macrophages are one of the first type of cells infected by the HIV virus when it enters the body.

Investigators at Temple University School of Medicine in Philadelphia assessed the impact of three commercially available synthetic THC agonists on HIV-infected macrophage cells. Following administration, researchers sampled the cells periodically to measure the activity of an enzyme called reverse transcriptase (RT), which is essential for HIV replication. By day 7, investigators reported that the administration of all three compounds was associated with a significant decrease in HIV replication.

Stated a Temple University news release: "The results suggest that selective CB2 (cannabinoid 2 receptor) agonists could potentially be used in tandem with existing antiretroviral drugs, opening the door to the generation of new drug therapies for HIV/AIDS. The data also support the idea that the human immune system could be leveraged to fight HIV infection."

Patients living with HIV/AIDS frequently report using cannabis to counter symptoms of anxiety, appetite loss, chronic pain, and nausea, and one study has reported that patients who consume cannabis therapeutically are 3.3 times more likely to adhere to their antiretroviral therapy regimens than non-cannabis users. In preclinical models, the long-term administration of delta-9-THC has recently been associated with decreased mortality and ameliorated disease progression in monkeys. In clinical models, cannabis inhalation is associated with decreased neuropathy and increased levels of appetite hormones in the blood of subjects with HIV infection.

For more information, please contact Paul Armentano, NORML Deputy Director, at: paul@norml.org. Full text of the study, "Attenuation of HIV-1 replication in macrophages by cannabinoid receptor 2 agonists," appears online in the Journal of Leukocyte Biology.