Associate Professor of Microbiology and Immunology
BiographyDr. Noula Shembade is a basic and translational virologist, associate professor tenured at the Department of Microbiology and Immunology Miller School of Medicine, University of Miami (UM). His research focused on elucidating the molecular mechanisms involved in the regulation of pathogenic infection-induced uncontrolled inflammation, which leads to autoimmune diseases and cancer. Oncogenic virus infection-mediated chronic inflammation that affects immune surveillance and responses to therapy. Inflammation is chronically activated in Adult T-cell leukemia/lymphoma (ATL or ATLL) triggered by human T-cell lymphotropic virus-1 (HTLV-1), primary effusion lymphoma (PEL) and multicentric Castleman's disease mediated by Kaposi's sarcoma-associated herpesvirus (KSHV), and Burkitt's lymphoma and Hodgkin's lymphoma caused by Epstein–Barr virus (EBV). Oncogenic virus infection has been shown to increase the risk of cancers in HIV/AIDS. About 30-40% of AIDS-related cancers in HIV+ individuals treated with antiretroviral drugs are caused due to oncogenic virus infection and in many circumstances they are incurable. Persistent activation of key transcription factors, including NF-?B and STATs, leading to the induction of chronic inflammation and survival factors is a critical mechanism for the development of oncogenic virus-associated malignancies in HIV/AIDS. Inflammation induced by STATs and NF-?B, in response to microbial pathogenic infections and ligand dependent receptors stimulation, is critical to control infections. However, uncontrolled inflammation induced by STATs and NF-?B in oncogenic virus infected cells leads to immune dysfunction, persistent infection, inflammatory related diseases, and the development of cancers. Dr. Shembade made numerous breakthroughs in identifying key mechanisms and host factors involved in the regulation of NF-?B and STATs activation. These findings will be used to identify drug targets for tumor virus-induced cancers. More recently, Dr. Shembade has been studding the molecular mechanism of Perforin-2 in the regulation of type I, II, and III IFN-mediated JAK/STAT signaling in pathogenic infected cells.
Dr. Shembade joined the Department of Microbiology and Immunology as a post-doctoral fellow in the summer of 2005, following the completion of his PhD in May 2005 at the Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany. In the summer of 2012, he was promoted to faculty in the Department of Microbiology and Immunology, UM, and in 2021, he was approved tenure at the rank of Associate professor.
Dr. Shembade teaches innate immunity, virology, and classes related to oncogenic virus-induced cancers to undergraduate and graduate students. Dr. Shembade’s research has been supported by American Cancer Society, Florida Biomedical Research Programs, and NIH.
Dr. Shembade has authored dozens of peer-reviewed research articles, some of which have been published in high-impact factor peer-reviewed journals and are widely cited in the field. Dr. Shembade serves on several peer review committees for scientific journals as well as national and international grant application review committees.
Education & Training
Post Graduate Training
Honors & Awards
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Teaching InterestsFor more than 10 years, my life has revolved around teaching undergraduate and graduate students. My teaching interests are also apparent in my research. My teaching philosophy strengthens as I gain experience teaching in various settings. My goal is for students to master in class and in the lab. This process begins with equipping students with the materials they'll need to succeed. Students must be taught current, rigorous, and proven theoretical frameworks and laboratory methods. This requires students acknowledging the advantages and pitfalls of various ideas as well as the complexity of the problems. In addition, students must be able to deal with ambiguity and limited resources. As a teacher, I assist students in identifying and resolving issues. Students frequently fail to recognize that the majority of their learning takes place when they are unable to effectively use tools. I assist students in recognizing this through project-based learning. Students can acquire knowledge quickly if frameworks and theories are designed to encourage them to consider complex problems. These frameworks and theories cannot be directly applied, but they can help students structure their thought processes when addressing complex problems. Undergraduates require more guidance due to their lack of experience, but I believe they would learn much faster than graduate students if given adequate resources, such as an interactive environment, providing feedbacks, and presentations. This type of hands-on, problem-based learning necessitates hearing different points of view, taking risks, and engaging in respectful debate. I believe it is my responsibility to ensure that these things are valued in the classroom. Setting a good example is one way to accomplish this. I try to involve everyone and demonstrate that I value what each student has to say. I'm also available to answer questions and discuss issues. In fact, if I'm being honest, I think what I learn from teaching is what I enjoy most about it. Debates in the classroom allow teachers to reconsider and revise their own ideas as needed. One of the things I enjoy most about teaching is the opportunity for both my students and myself to continue growing.
Research InterestsProject I: Molecular mechanisms of chronic inflammation regulation: Inflammation produced in response to microbial infection and tissue damage is critical to protect against infections across the board and organize long-term adaptive immunity against specific pathogens. Chronic and uncontrolled inflammation, on the other hand, typically causes major tissue damage and significant pathogenicity due to overactive immune responses. Shembade’s laboratory focuses on understanding the molecular mechanisms of chronic inflammation regulation in cancer cells, as well as inflammatory diseases and innate immune receptor stimulation.
Project II: Molecular mechanisms of NF-?B regulation in EBV, KSHV, and HTLV-infected cells: Chronic inflammation induced by NF-?B is essential for the survival of leukemia and lymphoma cells infected with oncogenic viruses, such as EBV, KSHV, and HTLV-1. Viral oncogenes, LMP-1 of EBV, vFLIP and vGPCR of KSHV, and Tax of HTLV-1, are hijacking and post-translationally modifying host factors to maintain chronic NF-?B activation in leukemias and lymphomas. However, the host factors that are post-translationally modified are not fully known. Thus, another focus of his laboratory is to identify the mechanisms and host factors that post-translationally modified by the viral oncogenes to maintain chronic NF-?B activation in leukemias and lymphomas.
Project III: Regulation of translation initiation during KSHV replication and oncogenesis: Despite advances in our understanding of KSHV pathogenesis and the implementation of rationally designed therapies based on these findings, advanced KS is largely incurable, and many of the most promising new therapies continue to face major roadblocks and implementation issues in the context of ART. KSHV regulate the oxygen sensing machinery allowed the virus to adjust the hypoxia-regulated alternative translation initiation machinery eIF4EH activated by HIF2a and mediated by eIF4E2 alternative cap-binding. This was essential for KSHV replication. Thus, 1: investigate how KSHV regulation of the oxygen sensing mechanism (O2SM), which results in HIF2a stimulation of translational initiation by eIF4EH, contributes to KSHV replication and innate immunity evasion; and 2: investigate how KSHV modulation of the oxygen sensing machinery, which results in HIF2a stimulation of translational initiation by eIF4EH, contributes to KSHV oncogenesis in mouse and human MSCs. 3: The role of translation initiation plasticity in PDGFRA targeted therapy resistance.
Project IV: Develop a KSHV oncogenesis mouse model in the HIV/AIDS setting: Pathogenesis-based treatment design and testing is hampered by a lack of adequate HIV/AIDS-specific KSHV oncogenesis models. In collaboration with the Dr. Roy Lab, we discovered that a) EcoHIV therapy of mECK36 (Bac36KSHV-infected) tumor-bearing nude mice promotes tumor cell proliferation, and b) EcoHIV infection of Balb/c mice allows grafting and growth of KSHV tumors. Thus, we want to know if "new in vitro and in vivo models of HIV/AIDS-associated malignancies can be developed to study their development, pathogenesis, and the potential evaluation of novel treatments for common HIV/AIDS-associated malignancies."
Project V: Regulation of type I and II interferons signaling: Type I interferons (IFN-a and IFN-ß) and type II interferon (IFN-?) are induced in response to infections with viruses or bacteria. IFNs bind to their cognate receptor, which plays important roles in host defense against invading pathogens. Type I interferons provide protection against many viral infections, whereas type II interferon is essential for host defense against some bacterial and parasitic pathogens. Interestingly, numerous studies have also found that functional dysregulation of either interferon response can lead to chronic pathological conditions associated with numerous human diseases, including tissue damage and autoimmu
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