Meth, crystal, Tina – regardless of the name, folks have long known that use of the street drug creates a kind of euphoria that can lead to increased risky behavior and contribute to the spread of HIV infection.

Now, researchers have shown a second way that meth increases the risk of infection and can speed up the pace of the disease. It is at the level of the virus interacting with the cells of the body.

Dr. Madhavan P.N. Nair, a cellular biologist at the University at Buffalo, looked at dendritic cells, part of the immune system that HIV – and other pathogens – first latch onto when entering the body.

He found that when meth attaches itself to dopamine receptors on cells, the action somehow causes more of the molecule DC-SIGN to express itself on the surface of cells. DC-SIGN is the receptor molecule on the surface of dendritic cells that HIV grabs on to near the surface of skin or mucosal tissue.

This complex of cells and virus then travels deeper into the immune system so that T-cells can kill the pathogen. T-cells can kill some HIV but they are overwhelmed by the increased number of virus that attaches to the meth-activated dendritic cells.

“This finding shows that using meth is doubly dangerous,” Dr. Nair said. “Meth reduces inhibitions, thus increasing the likelihood of risky sexual behavior and the potential to introduce the virus into the body, and at the same time allows more virus to get into the cell.”

Dr. Nair also said use of dopamine receptor blockers during HIV infection in meth users could “be beneficial therapeutically to reduce HIV infection in these high-risk populations.”

However, the practical problem is that meth’s action on the dopamine receptor also is responsible for all of the pleasurable effects that users seek from the drug. So they are not likely to use anything that negates that purpose.

Additional researchers on the publication, all from the UB Department of Medicine, are Supriya Mahajan, Ph.D., research assistant professor; Donald Sykes, Ph.D., research associate professor; Meghana V. Bapardekar, Ph.D., postdoctoral associate, and Jessica L. Reynolds, Ph.D., research assistant professor.

The study was published online on Aug. 4 in the Journal of Neuroimmune Pharmacology and will appear in print in the journal’s September edition.