The focus of my laboratory is the host response to human RNA viral infections such as Dengue and Coronavirus. RIG-I like receptor (RLR) pathway is a major innate immune response pathway in mammals, that recognizes double stranded RNA intermediates of replication in RNA viruses. Activation of type-I interferons (IFN) is the outcome of such response that is mediated through a key mitochondrial membrane-associated protein, MAVS. Beyond the sketches of these responses, deeper details of these regulations in various cell types are still missing. In one of our recent findings, we identified that epithelial-mesenchymal transition (EMT) is caused by a broad range of viruses and EMT-TFs are activated as part of RLR signalling that promotes antiviral state in a strong way. Various viral proteins are known to interfere with IFN signalling, neutralizing the pathway at multiple nodes. Our laboratory has been studying the delayed response of RLR pathway following SARS-CoV-2 infection in epithelial cells using infectious SARS-CoV-2 particles. Of particular interest is understanding the molecular mechanisms by which some of the recently evolved variants of the virus, such as Alpha- and Delta are able to replicate by evading the host innate immune system. Since host factors are key to the success of viral infection, their differential manipulation by distinct variants is an important aspect in these studies.
Krishnan, H.H., et al., 2004. Concurrent expression of latent and a limited number of lytic genes with immune modulation and anti-apoptotic functions by KSHV/HHV-8 early during infection of primary endothelial and fibroblast cells and subsequent decline of lytic gene expression. J Virology: 78:3601-20.
George, A., et al., 2012. Hepatitis C virus NS5A binds to the mRNA Cap binding eIF4F complex and upregulates host translation initiation machinery through 4EBP1 inactivation. J. Biol. Chemistry. 10; 287(7): 5042-58.
Panda, S., et al., 2014. Hepatitis C Virus Protein NS5A Coordinates a Unique Phosphorylation Dependent eIF4E Assembly on 40S Ribosomes That Regulates IRES Activity. Biochemical Journal, Sep 1;462(2):291-302.
Vedagiri, D., et al., 2016. An Atypical System for Studying Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma. Scientific Reports 6:26282
Parveen, S., et al., 2017. Unconventional MAPK-GSK-3? Pathway Behind Atypical Epithelial-Mesenchymal Transition In Hepatocellular Carcinoma. Scientific Reports 7, 8842 (2017)
Education & Experience
|P.G:||Biotechnology ; Cochin University of Science and Technology ; 1998|
|Ph.D:||Anaerobic regulation in V.cholerae ; Jadavpur/Indian Institute of Chemical Biology ; 2003|
Virology ; University of Kansas Medical Center ; 2002-2007
|Retinoic acid Inducible Gene-I like Receptors Activate Snail and Slug to Limit RNA Viral Infections.||J. Virology (Accepted)||2021|
|Inactivation of SARS-CoV-2 by Î²-propiolactone Causes Aggregation of Viral Particles and Loss of Antigenic Potential.||Virus Research.||2021|
|Easing diagnosis and pushing the detection limits of SARS-CoV-2||Biology Methods and Protocols||2020|
|mTORC1 Restricts Hepatitis C Virus RNA Replication Through ULK1-mediated Suppression of miR-122 and Facilitates Post-replication Events.||Journal of General Virology (2019). DOI 10.1099/jgv.0.001356||2019|
|An Atypical System for Studying Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma.||Sci Rep. 2016 May 20;6:26282. doi: 10.1038/srep26282.||2016|
|Hepatitis C Virus Protein NS5A Coordinates a Unique Phosphorylation Dependent eIF4E Assembly on 40S Ribosomes That Regulates IRES Activity.||Biochemical Journal 2014 Jun 4. PMID:24894874; doi:10.1042/BJ20131530).||2014|
|Hepatitis C virus NS5A binds to the mRNA Cap binding eIF4F complex and upregulates host translation initiation machinery through 4EBP1 inactivation. Journal of Biological Chemistry.||Journal of Biological Chemistry. 287, NO. 7, 5042||2011|
|Focal Adhesion Kinase (FAK) is critical for Kaposi's Sarcoma Associated Herpesvirus (KSHV-HHV-8) entry into the target cells.||J. Virology. 80. 1167-1180. (Selected in the J.Virology spotlight in the same issue)||2006|
|Envelope glycoprotein gB of Kaposi's sarcoma Associated Herpesvirus (KSHV/HHV-8) is essential for egress from infected cells||J. Virology. 79. 10952-10967.||2005|
|ERK1/2 and MEK1/2 induced by Kaposi's Sarcoma Associated Herpesvirus (KSHV/HHV-8) early during infection of target cells are essential for the expression of viral genes and for the establishment of infection.||J. Virology. 79. 10308-10329.||2005|
|Kaposi's sarcoma associated herpesvirus (KSHV/HHV-8) modulates the Microtubule Dynamics via RhoAGTP- Diaphenous-2 Signaling and Utilizes the Dynein Motors to deliver its DNA to the Nucleus.||J. Virology. 79. 1191-1206.||2005|
|Effect of anaerobiosis on expression of virulence factors in Vibrio cholerae.||Infection and Immunity. 72. 3961-3967.||2004|
|Kaposi's Sarcoma Associated Herpesvirus (KSHV/HHV-8) envelope glycoprotein gB induces the integrin dependent focal adhesion kinase-Src-PI-3K-RhoGTPase signal pathways and cytoskeletal rearrangements.||J.Virology. 78: 4207-4223.||2004|
|Concurrent expression of latent and a limited number of lytic genes with immune modulation and anti-apoptotic functions by KSHV/HHV-8 early during infection of primary endothelial and fibroblast cells and subsequent decline of lytic gene expression.||J Virology: 78:3601-20.||2004|
|Host gene induction and transcriptional reprogramming in KSHV/HHV-8 infected endothelial, fibroblast and B cells: Insights into modulation events early during infection.||Cancer Research; 64:72-84.||2004|
|Kaposi's sarcoma-associated herpesvirus induces Phosphatidylinositol 3-Kinase-PKC-?-MEK-ERK signaling pathway in the target cells early during infection: implications in infectivity||J.Virology. 77:1524-1539.||2003|