Rendezvous with Tat: Transactivator of Transcription during Human Immunodeficiency Virus Pathogenesis
Sneham Tiwari, Madhavan P.N. Nair and Shailendra K. Saxena
DOI : 10.3844/ajidsp.2012.79.91
American Journal of Infectious Diseases
Volume 8, Issue 2
Acquired immune deficiency syndrome is a deadly disease caused by HIV, declared as a global catastrophe engulfing millions of lives per year. It took ~1.8 million lives in the year 2010 alone, as per reports of UNAIDS. HIV-1 is an enveloped retrovirus, having genome composed of two copies of ssRNA. It attacks the T-lymphocytes of the hosts, causes several multifaceted immune failures and finally leads to fatality. Our articles focuses on small regulatory tat (transactivator of transcription) gene which is responsible for the initiation and elongation of viral transcription through the LTR transactivation. It consists of two exons combining to form protein of 101 amino acids that enhances the efficiency of viral transcription. Tat exon 1(1-72) is important for viral transcription and Tat exon 2 (73-101) is important for cell adhesion and several activities like cellular uptake of the exogenous Tat, apoptosis, improvement of HIV-1 replication and IL-2 super induction in HIV-1-infected T cells. Tat plays vital role in LTR transcription, reverse transcriptions, Kaposis sarcoma, neuropathogenesis, immunosuppression, concluding its importance. Eventually in future approaches, tat gene can be targeted for gene based drug targeting as Tat exon 1 is quite conserved and Tat exon 2 has important conserved motifs, which can behave as potent drug targets. Our review recommends to focus over tat gene, which might prove as a lead in HIV research, which should be treated with ssense of urgency.
© 2012 Sneham Tiwari, Madhavan P.N. Nair and Shailendra K. Saxena. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.