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Open AccessArticle

In-Vitro Subtype-Specific Modulation of HIV-1 Trans-Activator of Transcription (Tat) on RNAi Silencing Suppressor Activity and Cell Death

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Laboratory of Virology, National Institute of Immunology, New Delhi 110067, India
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Department of Microbiology, University College of Medical Sciences and Guru Teg Bahadur Hospital, Delhi 110095, India
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Ragon Institute of MGH, MIT and Harvard University, 400 Technology Square, Cambridge, MA 02139, USA
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Renal Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
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Department of Medical Biochemistry, Dr. A. L. M. Postgraduate Institute of Biomedical Sciences, University of Madras, Chennai, Tamil Nadu 600113, India
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Endocrinology & Toxicology Lab, Department of Zoology, University of Calicut, Kerala 673635, India
*
Authors to whom correspondence should be addressed.
Viruses 2019, 11(11), 976; https://doi.org/10.3390/v11110976
Received: 15 May 2019 / Revised: 6 October 2019 / Accepted: 9 October 2019 / Published: 23 October 2019
Human immunodeficiency virus (HIV) is a global health concern affecting millions of individuals with a wide variety of currently circulating subtypes affecting various regions of the globe. HIV relies on multiple regulatory proteins to modify the host cell to promote replication in infected T cells, and these regulatory proteins can have subtle phenotypic differences between subtypes. One of these proteins, HIV-1 Trans-Activator of Transcription (Tat), is capable of RNA interference (RNAi) Silencing Suppressor (RSS) activity and induction of cell death in T cells. However, the subtype-specific RSS activity and induction of cell death have not been explored. We investigated the ability of Tat subtypes and variants to induce RSS activity and cell death. TatB, from HIV-1 subtype B, was found to be a potent RSS activator by 40% whereas TatC, from HIV-1 subtype C, showed 15% RSS activity while subtype TatC variants exhibited varying levels. A high level of cell death (50–53%) was induced by subtype TatB when compared to subtype TatC (25–28%) and varying levels were observed with subtype TatC variants. These differential activities could be due to variations in the functional domains of Tat. These observations further our understanding of subtype-specific augmentation of Tat in HIV-1 replication and pathogenesis. View Full-Text
Keywords: human immunodeficiency virus (HIV)-1; trans-activator of transcription (Tat) gene; acquired immunodeficiency syndrome (AIDS); RNA interference (RNAi) silencing suppressor (RSS) activity and cell death human immunodeficiency virus (HIV)-1; trans-activator of transcription (Tat) gene; acquired immunodeficiency syndrome (AIDS); RNA interference (RNAi) silencing suppressor (RSS) activity and cell death
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Ronsard, L.; S. Yousif, A.; Ramesh, J.; Sumi, N.; Gorman, M.; G. Ramachandran, V.; C. Banerjea, A. In-Vitro Subtype-Specific Modulation of HIV-1 Trans-Activator of Transcription (Tat) on RNAi Silencing Suppressor Activity and Cell Death. Viruses 2019, 11, 976.

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