Profile
My research is to understand genetic basis of disease that includes infectious and complex disease. Currently my research focus is to understand the host response to tuberculosis using genomics. We are interested in deep mining of host genetic factors determining susceptibility to infection and understand pathogen and host interface using multiomics approach. Towards this we identified variants in SIGLEC15, HLA-DRA to associate with tuberculosis and chemokine CXCL10 as a marker for active disease. I am also interested in understanding genetic basis of congenital heart diseases both syndromic (Noonan Syndrome) and nonsyndromic (ASD, VSD etc).
Current Focus Areas
Host pathogen interaction in tuberculosis. We use genomic transcriptomic and functional approach to understand host response. We are also exploring on different cell death pathways induced during infection of M.tb. We are also interested on pathogen genomics to understand nature of mutations, drug resistant pattern etc
Understanding genetic basis of congenital heart diseases both syndromic (Noonan Syndrome) and nonsyndromic (ASD, VSD etc) and functional study of disease pathology
Selected Publications
• Pandit B., Bhattacharjee S., Bhattacharjee B. (2021) Association of clade-G SARS-CoV-2 viruses and age with increased mortality rates across 57 countries and India, Infection, Genetics and Evolution, 90. 104734
• Tonsing M.V., Sailo C.V., Zothansanga, Chhakchhuak L, Chhakchhuak Z, Pandit B, Kumar D, Mazumder PP, Senthil Kumar N. (2020) Analysis of variants in mitochondrial genome and their putative pathogenicity in tuberculosis patients from Mizoram, North east India. Mitochondrion. Sept 54:21-25.
• Bhattacharyya C, Majumder P.P., Pandit B. (2019) An exome wide association study of pulmonary tuberculosis patients and their asymptomatic household contacts, Infection, Genetics and Evolution, 71, 76-81.
• Bhattacharyya C, Majumder P.P, Pandit B., (2018) CXCL10 is overexpressed in active Tuberculosis patients compared to M. tuberculosis-exposed household contacts, Tuberculosis,)109:8-16
• Pandit B., Sarkozy A., Pennacchio L.A., Carta C., Oishi K,,Martinelli S., Pogna E.A., Schackwitz W., Ustaszewska A., Landstrom A., Bos J.M., Ommen S.R., Esposito G., Lepri F., Faul C., Mundel P., López Siguero J.P., Tenconi R., Selicorni A., Rossi C., Mazzan L., Torrente I., Marino B., Digilio M.C., Zampino G., Ackerman M.J., Dallapiccola B., Tartaglia M., Gelb B.D., (2007) Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy- Nature Genetics 39(8):1007-1012.