Rendezvous with Tat: Transactivator of Transcription during Human Immunodeficiency Virus Pathogenesis
Sneham Tiwari1, Madhavan P.N. Nair2 & Shailendra K. Saxena1 Show affiliations
- CSIR-Centre for Cellular and Molecular Biology, India
- Florida International University, United States
American Journal of Infectious Diseases, Volume 8, Issue 2, pp. 79–91 · doi.org/10.3844/ajidsp.2012.79.91
Abstract
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, Kaposi’s 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.
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Tiwari, S., Nair, M. P. & Saxena, S. K. (2012). Rendezvous with Tat: Transactivator of Transcription during Human Immunodeficiency Virus Pathogenesis. American Journal of Infectious Diseases, 8(2), 79–91. https://doi.org/10.3844/ajidsp.2012.79.91
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