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Debasis
Mondal, Ph.D.
Assistant Professor
Louisiana State University Health Sciences Center, New Orleans,
1995
Research Interests
Molecular mechanisms linked to HIV-1 induced pathogenesis. Role of HIV-1
transactivator (Tat) protein in regulating viral latency and infectivity.
Possible pharmacological interventions to enhance the efficacy and reduce
the toxic side effects of anti-retroviral drugs.
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Academic Training:
- M.S. Dept. of Biochemistry, LSUHSC, New Orleans, LA, 1989
- Ph.D. Dept. of Microbiology, Immunology and Parasitology. LSUHSC, New Orleans,
LA, 1995
- Post-doctoral Research -- Dept. of Pharmacology, TUHSC, New Orleans, LA,
1995-2002
- Research Assistant Professor -- Dept. of Pharmacology, TUHSC, New Orleans,
LA, 2002-2003
- Assistant Professor -- Dept. of Pharmacology, TUHSC, New Orleans, LA, 2003-present.
Address:
Department of Pharmacology SL83, Tulane University Health Sciences Center,
1430 Tulane Avenue, New Orleans, LA 70112.
Telephone: (504) 988-4668; Fax: (504)-988-5283; Email: dmondal@tulane.edu
Research Interests:
The focus of my research is to delineate the molecular mechanisms linked to
the persistence and pathogenesis of the AIDS virus (HIV-1) within viral sanctuary
sites such as the bone marrow, lymph nodes and the brain. Specifically, we are
trying to understand what makes HIV-1 ‘tick’, survive and evade
the actions of anti-retroviral drugs. We aim to elucidate the dynamic interactions
that occur between viral and host factors, which ultimately dictate viral latency,
infectivity and pathogenesis. We have observed that HIV-1 infected cells constitutively
express and secrete the trans-activator (Tat) protein of HIV-1. Dysfunctions
in different hematopoietic and mesenchymal cell lineages are frequently observed
in HIV-infected individuals. Our studies suggest that the paracrine actions
of Tat protein on different cellular microenvironments may play a crucial role
in manifestating virus-induced pathogenesis in tissue reservoirs of HIV-1. Our
studies have also shown that Tat protein can regulate HIV-1 co-receptor (CXCR4
and CCR5) expression in different hematopoietic cell types, which implicates
this viral factor as a crucial regulator of viral infectivity. In addition,
our current findings also show a direct association between Tat protein function
and the activity of certain host cell transcription factors which are required
for transcriptional activation of the HIV-1 long terminal repeat (LTR). Future
experiments will illuminate our understanding of how cellular activation signals
can regulate proviral activation in latent reservoirs. We believe that our findings
will facilitate the discovery of possible pharmacologic interventions to suppress
the disease progression to AIDS, and will lead to the development of more efficacious
anti-retroviral therapy.
Publications:
A listing of research
publications for Debasis Mondal.
Funding:
Pending Grants
- Board of Regents Support Fund (BORSF)-RCS proposal; Bone marrow stromal
cells, a sanctuary site for HIV-1 infection; Principle Investigator: Dr. D.
Mondal; 06/30/03-07/01/06; total direct cost 178,511; 20% effort.
- NIH-NIDDK; RFA DK-03-002; Anti-adipogenic effects of HIV-1 and Tat in human
MPCs. Principle Investigator: Dr. D. Mondal; 10/01/03-09/30/07; total direct
cost 1,485,000; 20% effort.
- NIH-NCI; R21 CA102915-01; Mesenchymal stromal cells in prostate cancer metastasis;
Principle Investigator: Dr. K.C. Agrawal, Co-investigator: Dr. D. Mondal;
07/01/03-06/30/05, total direct cost 297,000; 15% effort.
Ongoing Research Support
- NIH; RO1; Mechanisms of HAART induced endothelial dysfunctions; Principle
Investigator: Dr. K.C. Agrawal, Co-investigator: Dr. D. Mondal; 07/01/03-06/30/07,
total direct cost 1,485,000; 20% effort.
- Continuing involvement in three funded NIH grants (PI: Prof. K.C. Agrawal,
Ph.D.) awarded on studies towards the understanding of HIV-induced pathogenesis
and toxicities linked to anti-retroviral therapy.
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This page was last updated on April 3, 2007.