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Updated: Jun 24, 2026

Evaluation of the Efficacy And Toxicity of RNAs Targeting HIV-1 Production for Use in Gene or Drug Therapy
Published on: September 5, 2016
HIV regulation of amyloid beta production
1Veterans Affair Medical Center, San Francisco, University of California, San Francisco, CA 94121, USA. Lynn.Pulliam@ucsf.edu
Abstract:
The use of antiretroviral therapy for HIV infection has extended the survival of individuals living with HIV. However, the effects of chronic HIV infection and aging are introducing another facet of HIV complications. HIV therapy can calm the immune system and lower viral replication to undetectable but the virus is still present. In the brain, amyloid beta (Abeta) increases during normal aging but Abeta accumulation appears to accelerate in HIV infection. HIV Tat protein inhibits the major Abeta-degrading enzyme neprilysin with the cysteine-rich domain of Tat being essential for this inhibition. In this minireview, we also include new data that the beta chemokine, CCL2/MCP-1, associated with HIV migration to the brain, also causes an increase in Abeta. These findings may explain the continued cognitive dysfunction found in HIV-infected individuals controlled on antiviral therapy.
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