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Tat and amyloid: multiple interactions.

The demographics of HIV infection continue to evolve. New infections with HIVare now increasingly being seen in retirement communities affecting the elderly population [1]. Additionally, with effective antiviral therapy, patients infected as young adults continue to live longer and are approaching older age groups. This is particularly true of countries where HIV clade B infection is most prevalent, and where it is also clear that this clade of HIV is associated with a dementing illness. Even though large populations in Africa and Asia are infected with clade C virus, its ability to cause neurocognitive impairment remains unknown. As antiretroviral drugs are being introduced in these regions survival will improve. Current antiretroviral therapy is targeted against either viral protease or reverse transcriptase. These modes of therapy have no impact on Tat production once the cell is infected and proviral DNA has been formed. This maybe particularly important in the brain where the virus may be sequestered in glial cells and macrophages and may evolve over a period of time. Hence understanding the interactions of Tat with the aging brain maybe critically important.