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.

Selected Publications

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)