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Unwalla, Hoshang Jehangir

Title: Associate Professor

Email: hunwalla@fiu.edu

Curriculum Vitae

Department(s): Immunology

Dr. Unwalla obtained his Ph.D. at the National Institute of Immunology, Jawaharlal Nehru University, Delhi, India. He was recruited as a post-doctoral fellow in the laboratory of Dr. John Rossi at the Beckman Research Institute, City of Hope, Duarte CA. As a post-doctoral fellow his research involved designing gene therapy approaches to suppress HIV replication.

As a post-doctoral fellow, he was the awarded the prestigious Foundation for AIDS Research (amfAR) fellowship, one of the four awarded world- wide that cycle.  In 2008, he moved to the University of Miami as an Assistant Professor, research-track to develop a core facility for aptamers in Immunotherapy. Dr. Unwalla developed an interest in HIV and lung disease and in 2009 he branched his area of research to pulmonary medicine with a goal towards developing research projects in pulmonary complications in smokers and HIV patients. He received funding from the American Lung Association (ALA) and the Florida Department of Health to support his research. Currently, Dr. Unwalla is serving as an Associate Professor, tenure-track in the Department of Immunology and the Center for Personalized Nanomedicine at Florida International University. The National Institute of Health (NIH) and Flight Attendant Medical Research Institute (FAMRI) have funded his ongoing research.

Selected Publications

  1. Chinnapaiyan S, Parira T, Dutta R, Agudelo M, Morris A, Nair M, Unwalla HJ. HIV Infects Bronchial Epithelium and Suppresses Components of the Mucociliary Clearance Apparatus. PLoS One. 2017 Jan 6; 12(1):e0169161. PMCID: PMC5217953.
  2. Chinnapaiyan S, Unwalla HJ. Mucociliary dysfunction in HIV and smoked substance abuse. Front Microbiol. 2015 Oct 14;6:1052. PMCID: PMC4604303.
  3. Unwalla H.*, Ivonnet P., Dennis J., Conner G. and Salathe M. Transforming growth factor-β1 and cigarette smoke inhibit the ability of β2-agonists to enhance epithelial permeability. Am J Respir Cell Mol Biol. 2015 Jan; 52(1):65-74. PMCID: PMC4370252. (*Unwalla is corresponding author)
  4. Unwalla HJ, Horvath G, Roth FD, Conner GE, Salathe M. Albuterol Modulates its own Transepithelial Flux via Changes in Paracellular Permeability. Am J Respir Cell Mol Biol. 2012 Apr; 46 (4):551-8. PMCID: PMC3359945.
  5. Unwalla H and Rossi JJ. Screening Effective Target Sites on mRNA: A Ribozyme Library Approach. Methods Mol Biol. 2012; 848:329-36. PMID: 22315078.
  6. Unwalla H, and Rossi JJ. A dual function TAR Decoy serves as an anti-HIV siRNA delivery vehicle. Virol J. 2010 Feb 10; 7: 33. PMCID: PMC2836314.
  7. Unwalla HJ, Li H, Li SY, Abad D, Rossi JJ. Use of a U16 snoRNA-containing ribozyme library to identify ribozyme targets in HIV-1. Mol Ther. 2008 Jun; 16(6):1113-9. PMCID: PMC2775071.
  8. Sood V*, Unwalla H*, Gupta N, Chakraborti S, Banerjea AC. Potent knock down of HIV-1 replication by targeting HIV-1 Tat/Rev RNA sequences synergistically with catalytic RNA and DNA. 2007 Jan 2;21(1):31-40. PMID: 17148965. (*Unwalla and Sood both first author with equal contribution)
  9. Unwalla H, Chakraborty S., Sood V., Gupta N., and Banerjea A.C. Potent inhibition of HIV-1 gene expression and Tat mediated apoptosis in human T cells by novel mono- & multitarget anti-TAT/Rev/Env ribozymes and a general purpose RNA-cleaving DNA- enzyme. Antiviral Res. 2006 Nov; 72(2):134-44. PMID: 16790281.
  10. Unwalla, H, Li, H.T., Bahner, I., Li, M-J., Kohn, D. and Rossi, J. J. A Pol II fusion promoter directs HIV-1 inducible co-expression of an shRNA and protein. J Virol. 2006 Feb; 80(4):1863-73. PMCID: PMC1367144.
  11. Unwalla, H, Li, M-J., Kim, J.D., Li, H.T., Ehsani A., Alluin J. and Rossi, J.J. Negative feedback inhibition of HIV-1 by TAT-inducible expression of siRNA. Biotechnol. 2004 Dec; 22(12):1573-8. PMID: 15568018.
  12. Unwalla, H, Banerjea, A. C. Inhibition of HIV-1 specific gene expression by novel macrophage-tropic DNA enzymes targeted to cleave HIV-1 TAT/Rev RNA. Biochem J. 2001 Jul 1; 357(Pt1):147-55. PMCID: PMC1221937.

Complete List of Published Work in My Bibliography:

http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/48296501/?sort=date&direction=ascending

Research Areas

Dr. Unwalla’s current research interests are primarily focused on understanding the pathophysiological mechanisms that lead to tracheobronchial mucociliary dysfunction in smokers and HIV patients with a goal towards developing therapeutics to restore MCC in these diseases.

         In aging HIV-infected populations comorbid diseases are important determinants of morbidity and mortality. Combination antiretroviral therapy has made HIV a treatable disease. However, HIV patients die of non-AIDS comorbidities almost a decade earlier that their non-HIV counterparts. Lung diseases such as COPD, pulmonary hypertension, and pneumonia are emerging as significant comorbidities in the HIV-infected population This is exacerbated in HIV patients who are addicted to nicotine and smoke tobacco. HIV-infected patients with an episode of pneumonia also often demonstrate a permanent decline in lung function. Pulmonary infection also induces recruitment and activation of immune cells leading to de novo infection of target cells and enhanced HIV replication. Thus, bacterial pneumonia can also contribute to HIV progression.

The etiology of HIV pneumonias is very similar to that observed in pneumonias associated with chronic airway diseases like cystic fibrosis and chronic bronchitis associated with smoking. Impaired mucociliary clearance is a hallmark of these diseases. HIV proteins and cigarette smoke suppress important components of the mucociliary clearance apparatus and TGF-beta signaling plays a prominent role in the process. The laboratory research focuses on understanding the pathophysiological mechanisms that lead to microbial colonization of the airways in HIV-infected patients and testing therapeutic leads to rescue MCC dysfunction in the context of HIV infection and CS with a long-term goal towards preventing recurrent lung infections in people living with HIV. To accomplish these goals Dr Unwalla’s laboratory is currently working on three different projects.

  • Role of TGF-b signaling in mucociliary dysfunction in smokers and COPD patients
  • Tracheobronchial mucociliary dysfunction in HIV patients
  • Developing aptamer-siRNA chimeras as therapeutics in airway diseases