Meth Knocks Down Immune Defense
It has recently become popular among gay and bisexual men to consume very high levels of Meth. At the same time there is a new population of HIV+ men who are developing AIDS over months instead of years as typical.
Unsafe sex together with Meth abuse have been incriminated as reasons for rapid disease progression. While studies show exacerbated AIDS symptoms and disease progression in HIV+ Meth abusers, the molecular mechanism is yet unknown. It was assumed, yet unproven, that the rapid disease progression might be due to a mutant “superstrain” of HIV that was extremely virulent. Unsafe sex has been the other issue hold as culprit for rapid progression, although this would not explain the more rapid time course of the disease.
Recent reseach now demonstrates demonstrates the first direct evidence that Meth is blocking immune response, and that the molecular mechanism of this immunosuppression is due to the collapse of acidic conditions in cells of the immune system, inhibiting the functions of antigen uptake and processing. These effects compromise the immune response to opportunistic infections and HIV.
These findings could have a major impact on public health, as there are over 35 million Meth abusers worldwide
Tallóczy Z, Martinez J, Joset D, Ray Y, Gácser A, et al. (2008)
Methamphetamine Inhibits Antigen Processing, Presentation, and Phagocytosis.
PLoS Pathog 4(2): e28 doi:10.1371/journal.ppat.0040028
Methamphetamine (Meth) is abused by over 35 million people worldwide. Chronic Meth abuse may be particularly devastating in individuals who engage in unprotected sex with multiple partners because it is associated with a 2-fold higher risk for obtaining HIV and associated secondary infections. We report the first specific evidence that Meth at pharmacological concentrations exerts a direct immunosuppressive effect on dendritic cells and macrophages. As a weak base, Meth collapses the pH gradient across acidic organelles, including lysosomes and associated autophagic organelles. This in turn inhibits receptor-mediated phagocytosis of antibody-coated particles, MHC class II antigen processing by the endosomal–lysosomal pathway, and antigen presentation to splenic T cells by dendritic cells. More importantly Meth facilitates intracellular replication and inhibits intracellular killing of Candida albicans and Cryptococcus neoformans, two major AIDS-related pathogens. Meth exerts previously unreported direct immunosuppressive effects that contribute to increased risk of infection and exacerbate AIDS pathology.