Journal of Neuroimmune Pharmacology

, Volume 4, Issue 2, pp 213–217

HIV Regulation of Amyloid Beta Production

Invited Review

DOI: 10.1007/s11481-009-9151-9

Cite this article as:
Pulliam, L. J Neuroimmune Pharmacol (2009) 4: 213. doi:10.1007/s11481-009-9151-9


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 (Aβ) increases during normal aging but Aβ accumulation appears to accelerate in HIV infection. HIV Tat protein inhibits the major Aβ-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 β chemokine, CCL2/MCP-1, associated with HIV migration to the brain, also causes an increase in Aβ. These findings may explain the continued cognitive dysfunction found in HIV-infected individuals controlled on antiviral therapy.


HIVTatCCL2MCP-1amyloid betabrain

Copyright information

© Springer Science+Business Media, LLC 2009

Authors and Affiliations

  1. 1.Veterans Affair Medical Center, San FranciscoUniversity of CaliforniaSan FranciscoUSA