HUMAN IMMUNODEFICIENCY VIRUS-1 TAT MEDIATED ELICITATION OF NEUROTOXICITY AND NEUROAIDS

P.T. AGRAWAL¹, S. TIWARI², S.K. SAXENA³, M.P. NAIR⁴, S. PILAKKA-KANTHIKEEL^5
1CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad- 500 007, AP, India.
²CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad- 500 007, AP, India.
³CSIR-Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad- 500 007, AP, India.
⁴College of Medicine, Florida International University, Miami 33199, FL, USA.
⁵College of Medicine, Florida International University, Miami 33199, FL, USA.

Received : 07-11-2013     Accepted : 05-06-2014     Published : 11-09-2014
Volume : 3     Issue : 2       Pages : 76 - 79
J Pathol Res 3.2 (2014):76-79

Keywords : HIV-1, Tat (transactivator of transcription), reverse transcription, apoptosis, neuropathogenesis, HAD, HAND, BBB, neuroAIDS, Tat, NMDAR
Conflict of Interest : None declared

Human immunodeficiency virus-1 (HIV-1) Tat induces the replication of HIV by alleviating the transcription of viral genes. Tat is re-leased from HIV infected cells and it modifies the functions of uninfected cells. HIV infected cells enter the brain through BBB. In the brain, Tat induces neuronal damage and leads to neuroAIDS. Oxidative stress is believed to play an important role for causing HIV-dementia. NeuroA-IDS is more common in aged HIV positive adults and drug abusers.