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Research Scientist D
sankar [at] thsti [dot] res [dot] in
Master of Science from the Department of Botany, University of Calcutta, West Bengal
Ph.D. in Molecular Virology from the Indian Institute of Science, Bangalore, Karnataka
Post-doctoral researcher in the Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland
Senior Research Associate, Centre of Excellence in Hepatitis C virus research, Indian Institute of Science, Bangalore, Karnataka
Research Scientist-C, Translational Health Science and Technology Institute, NCR Biotech Science Cluster

In India human pathogenic flaviviruses, including Japanese encephalitis virus and Dengue virus are responsible for a significant number of death and long-term debility. In spite of a similar genomic organization and mode of dispersal (through mosquito bite during blood meal), the pathogenic outcome of infection is unique to each virus. We study the cellular and molecular events following flavivirus infection in order to gain insight into the mechanism of their pathogenesis. The goal of these studies is to understand the molecular basis of the pathogenesis so that therapeutic strategies using novel or repurposed drugs can be designed.

Japanese encephalitis virus (JEV)

Every year, viral encephalitis caused by JEV infection leads to massive number of child deaths in endemic regions of our country. Further, many survivors are forced to bear with lifelong neurological defects. An acute infection-induced inflammatory response is implicated to cause damage to neurological tissues.  In addition to innate anti-viral inflammatory response JEV infection also induces an Unfolded Protein Response (UPR) in infected host cells by overwhelming the folding capacity of the Endoplasmic reticulum (ER).  Recent studies in multiple contexts show an extensive cross-talk between these two cellular response pathways. Also UPR promotes apoptotic death of infected cells. In addition to virus infection UPR is also implicated in aetiology of diverse non-infectious diseases like Pancreatitis, Diabetes and Inflammatory bowel disease (IBD). We study UPR in context of JEV infection to understand,  

1.      If UPR-associated cellular and molecular changes affects virus replication in a positive or negative manner

2.      How UPR signalling influences inflammatory response during JEV response?

So far, we have observed UPR to have a positive effect on virus replication through a promotion of viral protein synthesis (Journal of General Virology, 2014). The mechanism of this effect is however not clear yet (Frontiers in Microbiology, 2014). Interestingly, a parallel study showed that Autophagy, which is also induced by JEV infection, has a negative effect on JEV infection (Autophagy, 2014). In parallel, observation we have shown the expression of long non-coding RNAs to be regulated during UPR, with unknown consequences (Scientific Reports, 2015).  Presently we are trying to understand the connection between UPR and Autophagy in context of virus infection.      

Dengue virus

Dengue virus infection causes a potentially fatal febrile illness in large parts of the world especially south-Asian countries. The virus spreads through mosquito bite and the disease manifests either as a mild fever or progressively critical syndromes termed as Dengue haemorrhagic fever (DHF) and Dengue shock syndrome (DSS). DHF and DSS are characterized by leakage of plasma out of blood vessels leading to reduction in blood volume and an acute drop in platelet levels or thrombocytopenia. The latter is presumed to be responsible for spontaneous mucosal bleeding observed in DHF/DSS patients. Dengue associated thrombocytopenia has been hypothesized to be the consequence of both a drop in biogenesis of platelets and an increase in decay of platelets. We are exploring the feasibility and mechanistic details of both the mechanisms (Scientific Reports, 2017). We believe an understanding of these mechanisms would help devise therapeutic strategies for the mitigation of thrombocytopenia.



  • Ojha A, Nandi D, Batra H, Singhal R, Annarapu GK, Bhattacharyya S, Seth T, DarL, Medigeshi GR, Vrati S, Vikram NK, Guchhait P. Platelet activation determines the severity of thrombocytopenia in dengue infection. Scientific Reports (2017) Jan31;7:41697
  • Bhattacharyya S, Vrati S. The Malat1 long non-coding RNA is upregulated by signalling through the PERK axis of unfolded protein response during flavivirus infection. Scientific Reports (2015) Dec 4;5:17794
  • Sharma M, Bhattacharyya S, Nain M, Kaur M, Sood V, Gupta V, Khasa R, Abdin MZ, Vrati S, Kalia M. Japanese encephalitis virus replication is negatively regulated by autophagy and occurs on LC3-I- and EDEM1-containing membranes. Autophagy. (2014) Jul 16;10(9).
  • Bhattacharyya S. Can't RIDD off viruses. Frontiers in Microbiology (2014) Jun 18;5:292
  • Bhattacharyya S, Sen U, Vrati S. The RIDD pathway is activated during Japanese encephalitis virus-induced unfolded protein response and benefits viral replication. Journal of General Virology. (2014) Jan;95(Pt 1):71-9 PubMed PMID: 24114795.
  • Verma B, Bhattacharyya S, Das S. Polypyrimidine tract-binding protein interacts with coxsackievirus B3 RNA and influences its translation. Journal of General Virology. (2010) May;91(Pt 5):1245-55.
  • Zipprich JT, Bhattacharyya S, Mathys H, Filipowicz W. Importance of the C-terminal domain of the human GW182 protein TNRC6C for translational repression. RNA. (2009) May;15(5):781-93.
  • The structure and function of a cis-acting element located upstream of the IRES that influences Coxsackievirus B3 RNA translation. Bhattacharyya S, Verma B, Pandey G, Das S. Virology. (2008) Aug 1;377(2):345-54
  • Bhattacharyya S, Das S. An apical GAGA loop within 5' UTR of the coxsackievirus B3 RNA maintains structural organization of the IRES element required for efficient ribosome entry. RNA Biology. (2006) Apr;3(2):60-8
  • Bhattacharyya S, Das S. Mapping of secondary structure of the spacer region within the 5'-untranslated region of the coxsackievirus B3 RNA: possible role of an apical GAGA loop in binding La protein and influencing internal initiation of translation. Virus Research. (2005) Mar;108(1-2):89-100
  • Bhattacharyya S, Vrati S. The Malat1 long non-coding RNA is upregulated by signalling through the PERK axis of unfolded protein response during flavivirus infection. Sci Rep. 2015 Dec 4;5:17794.