Suvendu Ojha

Icompleted my PhD at BRIC-Institute of Life Sciences, Bhubaneswar, in 2025 and continue there as a Research Associate. My doctoral work asked how Staphylococcus aureus uses multidrug efflux systems to survive antibiotic exposure, how those systems are wired into global transcriptional regulators such as MgrA, and whether that machinery can be switched off pharmacologically. Answering it meant building the whole chain of evidence myself — screening approved-drug and LOPAC libraries, tracing hits back to the regulators controlling pump expression, measuring direct protein–ligand binding by calorimetry and spectroscopy, reading out membrane energetics and biofilm consequences by flow cytometry and confocal microscopy, and finally asking in murine infection whether restored susceptibility survives contact with a host. Two compound series from that work became Indian patents, one granted in 2026.

My interests now sit a layer above any single pump. What holds my attention is the question of why a genetically susceptible organism can still survive treatment, and the physiology that decides it: nucleotide second messengers — c-di-AMP, c-di-GMP, (p)ppGpp — and the growth, stress and persistence programmes they control; bacterial metabolism and the metabolic adaptations that accompany infection, including metabolic vulnerabilities that might themselves be drug targets; antibiotic tolerance and persistence as phenomena genuinely distinct from resistance; and biofilms as a physiological state rather than a phenotype, particularly where biofilm physiology, metabolism and reduced susceptibility meet in chronic infection.

I am equally drawn to polymicrobial infection — how species compete, cooperate, signal and exchange metabolites when they share a host niche, and how any of that alters antibiotic susceptibility. Alongside it sits the regulatory biology that connects virulence, stress responses and survival: quorum sensing, global regulators, and the networks that let a cell change what it is doing in response to what is happening around it.

Running through all of it is a preference for mechanistic questions that keep a translational end attached. Efflux inhibitors, potentiators and adjuvants, metabolic and signalling targets, and repurposed compounds are the fastest route from a finding to something usable — and, just as importantly, they force honesty about whether a proposed mechanism actually matters in a living host. Alongside my own projects I have trained five doctoral and master's researchers at the bench, which I have come to enjoy more than I expected.