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Rajeev Kaul

Assistant Professor
Department of Microbiology
Biotech Building, Ground Floor
University of Delhi South Campus

Ph: 011-24157328
Email: rkaul@south.du.ac.in
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  Education
BVSc & AH (1997), CCS Haryana Agricultural University, Hisar
MVSc (1999), CCS Haryana Agricultural University, Hisar
PhD (2004), Indian Veterinary Research Institute (Deemed University), Izatnagar
Postdoctoral (2004-10) University of Pennsylvania, Philadelphia, USA
Description of Research Expertise

Research interest: Molecular Biology of tumor associated viruses, Development of new generation vaccine against Veterinary viruses.

Key words: oncogenesis, viruses and cancer, viral oncology, Tumor Virology, Inflammation, Kaposi's Sarcoma, Epstein-Barr Virus, Hepatitis C virus, PPRV, vaccine, Immunesuppression

Description of Research:

Our lab is presently working to study biology of cancers mediated by viruses. 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 two human tumor associated viruses, one Epstein Barr Virus (EBV) and other 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.

Primarily, we study two human tumor associated viruses, one Epstein Barr Virus (EBV) and other Hepatitis C Virus (HCV). EBV is associated with a number of human cancers. EBV infects cells and remains hidden in latent form. Long term inflammation has been linked to various steps involved in generation of cancer. We are trying to investigate a direct link between chronic long term inflammation and progression of EBV associated cancers. This study will also provide an explanation as to what causes the increased risk of cancer (lymphoma) in people who develop conditions such as rheumatoid arthritis considering that chronic inflammation and not the anti-inflammatory treatments using COX inhibitors has been found to be connected to lymphoma risk in rheumatoid arthritis patients.


EBV latent infection modulates COX-2 mediated functions via Nm23-H1 (Kaul et.al., J Virol. 80(3):1321-31.)

In a separate study, we are working to understand the role of Cox-2 in Hepatitis C Virus (HCV) pathogenesis. We hypothesize that Cox-2 is one of the HCV triggered pathogenic factors with key roles in inflammation, neo-angiogenesis, cell proliferation, and invasion associated with the HCC lesions. The central theme of this project is to elucidate the role of mediator of inflammation Cox-2 in HCV pathogenesis. Understanding the mechanisms governing the modulation of inflammatory molecules by HCV proteins will contribute to understanding of HCV’s role in hepatocellular carcinoma. This study is an attempt to investigate a direct link between chronic inflammation characterized by upregulated Cox-2 levels and progression of HCV associated hepatic cancer. The identification of cellular pathways critical for this regulation will also help devise novel strategies for therapeutic intervention in such patients.

HCV infection plays a critical role in regulation of Cox-2 expression, which is important for HCV pathogenesis and HCV mediated tumorigenesis.


In addition, We have recently initiated work on understanding the molecular basis of peste-des-petits ruminants (PPRV) mediated host immune modulation for the development of next generation vaccine. Immunosuppression and innate immunity control by morbilliviruses such as PPRV in small ruminants and measles in humans 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.



Health of small ruminants is critical for economic sustainability of our rural hinterlands  (A shepherd in Nubra valley, Ladhak 2016)

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