Prof. Rajeev Kaul
Professor
Head of the Department
& Dean of Faculty of Interdisciplinary & Applied Sciences
Fellow of Indian Virological Society
Biotech Building, Ground Floor
University of Delhi, South Campus
Benito Juarez Road, Delhi-110021
Email: rkaul@south.du.ac.in
Phone: 011-24157328 (Lab), 24157368 (Office)
Area of research: Microbial pathogenesis
Research description:
Our lab has worked to study biology of cancers mediated by viruses, and molecular basis of virus mediated host immuno-suppression. Tumor viruses have provided relatively simple genetic systems, which can be manipulated for understanding the molecular mechanisms of the cellular transformation process. A growing body of information in the tumor virology field provides several prospects for rationally targeted therapies. However, further research is needed to better understand the multiple mechanisms utilized by these viruses in cancer progression in order to develop therapeutic strategies. The major focus of our lab is to investigate virus host interactions using various tools including cell culture system and mice models. Primarily, we study three human tumor associated viruses, Epstein Barr Virus (EBV), Kaposi sarcoma associated herepesvirus (KSHV), and Hepatitis C Virus (HCV). In particular, we are using genetic, genomic, proteomic and biochemical approaches to identify viral pathways involved in these cellular events to develop mechanistic models for transformation by viruses. Tumor associated viruses provide a unique opportunity to understand the role played by viral proteins in transformation and to identify pathways critical for tumorigenesis and metastasis. A clear understanding of the pathways most critically involved in tumor formation and progression and the consequences of altered cell behavior in the tissue micro-environments will provide nuggets of information which will help us in formulating better therapeutic approaches. It is likely that a combination of therapeutic agents targeting multiple signal transduction pathways will be needed for maximum therapeutic benefits.
In addition, we have been working on understanding the molecular basis of peste-des-petits ruminants virus (PPRV) mediated host immune modulation for the development of next generation vaccine. Immuno-suppression and innate immunity control by morbilliviruses such as PPRV in small ruminants and measles in human remains a leading cause of death among infected host because it suppresses immune function, facilitating secondary infections. The basic mechanisms underlying PPRV-induced immunosuppression are poorly understood. The extent of viral replication documented in immune cells implies that it can directly cause immunosuppression. Our central hypothesis is that these viruses have evolved a multi-pronged host cell control strategy that allow them to replicate to high levels in host cells and induce generalized immunosuppression by interfering in cellular immune signaling pathways. The work will be important for more comprehensive understanding of basic cellular processes, in addition to providing us with targets to focus for development of anti-viral therapeutics and better safer non-immunosuppressive vaccines. The implications of the generated knowledge will extend beyond the morbillivirus field to include immunology, and cell biology. Small genome, simple organization and life cycle of morbilliviruses permits their use as a tool to dissect complex cellular pathways and to determine basic aspects of immune response induction. The research will lead to generation of information which can be used for development of approaches resulting in improvement of animal health and herd immunity.
Select Publications:
Yash Chaudhary, Purnati Khuntia, Rajeev Kaul (2022). Susceptibility to foot and mouth disease virus infection in vaccinated cattle, and host BoLA A and BoLA DRB3 genes polymorphism. VirusDisease. 2022 https://doi.org/10.1007/s13337-021-00754-8
Yashu Sharma, Roman Sarkar, Ayush Jain, Sudhakar Singh, Chander Shekhar, Chandrasekar Shanmugam, Muthuchelvan Dhanavelu, Prabhakar Tembhurne, Rajeev Kaul (Co-corresponding author), Sharvan Sehrawat (2021). A Mouse Model of PPRV Infection for Elucidating Protective and Pathological Roles of Immune Cells. Front Immunol. 2021 Apr 12;12:630307
Derek Gatherer, Daniel P. Depledge, Carol A. Hartley, Moriah L. Szpara, Paola K. Vaz, Mária Benkő, Curtis R. Brandt, Neil A. Bryant, Akbar Dastjerdi, Andor Doszpoly, Ursula A. Gompels, Naoki Inoue, Keith W. Jarosinski, Rajeev Kaul, Vincent Lacoste, Peter Norberg, Francesco C. Origgi, Richard J. Orton, Philip E. Pellett, D. Scott Schmid, Stephen J. Spatz, James P. Stewart, Jakob Trimpert, Thomas B. Waltzek, Andrew J. Davison, and ICTV Report Consortium (2021). ICTV Virus Taxonomy Profile: Herpesviridae. Journal of General Virology 2021 Oct: 102(10):001673.
Jain J, Gaur S, Chaudhary Y, Kaul R (2020). The molecular biology of intracellular events during Coronavirus infection cycle. VirusDisease 2020 May 4 : 1–5. 2020
Rajeev Kaul, Pravinkumar Purushothaman, Timsy Uppal and Subhash C. Verma (2019). KSHV lytic proteins K-RTA and K8 bind to cellular and viral chromatin to modulate gene expression. PLOS One, Apr 18;14(4):e0215394. doi: 10.1371/journal.pone.0215394
Catrherine Paul, Lohit Khera, Rajeev Kaul (2019). Hepatitis C virus core protein interacts with cellular metastasis suppressor Nm23-H1 and promotes cell migration and invasion. Arch Virol. 2019 Mar 11. doi: 10.1007/s00705-019-04151-x.
Nivedita Gaur, Tanvi Tikla, Rajeev Kaul (2018). Kaposi sarcoma‑associated herpes virus (KSHV) latent protein LANA modulates cellular genes associated with epithelial‑to‑mesenchymal transition. Arch Virol. https://doi.org/10.1007/s00705-018-4060-y.
Lohit Khera, Catherine Paul, Rajeev Kaul (2017). Hepatitis C Virus E1 protein promotes cell migration and invasion by modulating cellular metastasis suppressor Nm23-H1. Virology. 506:110-120