Project : Specific single domain antibodies (sdAbs) against antimicrobial resistant Mastitis pathogens for clinical therapeutic use in dairy animals
Funded by: DBT (~59.6 lakhs)
Period: Mar 2022-Mar 2025
Project : Center of Antibody Engineering: Center for Immuno-Diagnostics/ Therapeutics Veneering technologies (CIVET)
Funded by: DST-SERB (~187 lakhs)
Period: Mar 2022-Mar 2025
Project : Understanding the molecular basis of peste-des- petits ruminants virus (PPRV) mediated host immune modulation for the development of next generation vaccine
Funded by: ICAR-NASF (~59 lakhs)
Period: Apr 2017-Mar 2020
Overview: The PPRV infection leads to immunosuppression of the host and results in fatal secondary infections. We hypothesize that PPRV encoded proteins interfere with IFN signaling in host cell by modulation of JAK-STAT pathway, and contribute to the inhibition of adaptive immune responses leading to immuno-suppression in host. We are working to identify the specific PPRV encoded protein/ proteins responsible for modulation of IFN signaling, and immune pathway genes which are modulated by PPRV. We are also working to identify specific host proteins which interact directly with PPRV using proteomics approach.
Project: Molecular Surveillance of animal viral pathogens prevalent in Leh-Ladakh region
Funded by: DRDO (~10 lakhs)
Period: Sep 2015 - Sep 2017
Outcome: The viral antigens was not detected in any of the animal’s samples which were tested; however the detection of presence of antibodies against viral antigens clearly indicates that animals were exposed to virus infection. The variations in the sequence of BolA DRB3 gene in cattle correlated with the susceptibility of cattle to get infected with FMV virus in spite of being vaccinated. All the infected animals showed three different single nucleotide polymorphism in exon 2 of BoLA DRB3 gene, resulting in amino acid changes in peptide binding cleft of the protein. It is possible that presence of such changes exerts a significance impact on the peptide binding affinity of BoLA Class II molecule. And this differential binding might be affecting downstream immune response.
Project: Generation and characterization of a panel of Epstein Barr Virus transformed lymphoblastoid cell lines of diverse origin
Funded by: UGC (~13 lakhs)
Period: Jul 2012 – Dec 2015
Outcome: The project work resulted in generation of lymphopblastoid cells lines as a reagent for research usage. These cells were subsequently used to investigate role of Cox-2 in EBV lytic reactivation. The work showed that Cox-2 can induce lytic reactivation of EBV in latently infected cancer cells. This work is now being taken forward to identify the molecular pathways involved in the process and the lymphoblastoidc cells generated in the project are being used for these studies.
Project: Hepatitis C Virus infection and Expression of COX-2
Funded by: DBT (~54 lakhs)
Period: Apr 2012 – Oct 2015
Our studies show that HCV proteins NS4b and Core can upregulated COX-2 transcriptionally which is mediated via transcriptional factor NF-kB in case of HCV 4b. More importantly, we show that HCV-Core can directly interact with cellular metastasis suppressor Nm23-H1 and can rescue cancer cells from Nm23-H1 mediated suppression of metastasis. This clearly shows the role of HCV-Core in HCV mediated cancer metastasis. More importantly, we showed that HCV-Core can directly interact with cellular metastasis suppressor Nm23-H1 and can rescue cancer cells from Nm23-H1 mediated suppression of metastasis. Our studies also showed the role of HCV envelope protein E1 in downregulation of Nm23H1 expression by promoting its degradation thereby reducing its half-life and also transcriptional downregulation, resulting in promotion of cancer metastasis. We have published 2 papers (1 in Virology, 1 in Virus disease) and 1 has been submitted for publication in ‘Virology’.
Project: Mechanism of Epstein Barr Virus (EBV) latency control by Inflammation
Funded by: DBT (~40 lakhs)
Period: Jun 2011 to Dec 2014
LPS treatment as model system to deduce role of COX-2 expression on EBV latency in in EBV positive lymphoblastoid cells was developed and standardized. We showed that COX-2 over-expression resulted in lytic reactivation of EBV in latently infected cells. EBV progeny virions produced as a result of COX-2-mediated lytic reactivation were shown to be biologically active thereby confirming the biological significance of COX-2 mediated EBV lytic reactivation in tumorigenesis.A part of the work carried out in this project has already been published as na original research article in the journal “Virology”.