While at the Center she worked on Group A Streptococcus (GAS) is a spherical, gram-positive bacterium that is responsible for numerous diseases with diverse clinical manifestations specifically in humans. GAS likely plays a role in global health issues such as impetigo, pharyngitis, scarlet fever and life-threatening diseases such as necrotizing fasciitis, toxic shock, acute post-streptococcal glomerulonephritis, acute rheumatic fever and rheumatic heart disease. The pathogenesis of invasive GAS infections involves several stages e.g., adhesion to epithelial surfaces, colonization, transmigration of the bacteria through the epithelium and subepithelium, survival in blood, penetration through the endothelium, and invasion into deep tissue. To accomplish these steps, GAS possesses numerous genes encoding virulence factors, many of which need to be transcribed and/or repressed at specific stages of infection. The multiple gene activator (mga) system is one of the best-studied regulators that activate and inactivate genes rapidly in GAS under changing environmental conditions. The cluster of virulence (cov) intracellular responder (covR)/extracellular sensor (CovS) system (covRS) is a two-component sensor/responder gene regulatory system in GAS that regulates repression and depression of ~15% of the GAS genome. At several stages of dissemination of GAS, this microorganism must develop strategies to evade the host innate immune system, especially complement-mediated elimination of the microbe in order to survive. Our studies have implicated CovRS in regulating the opsonophagocytosis of GAS by the host complement system which is a part of innate immune system. Therefore, my primary focus of interest is to study the regulation of bacterial opsonophagocytosis by the CovRS regulatory system.
Her final thesis was entitled "Two-Component CovRS Regulatory System: Role In Host Innate Immunity Modulation And Bacterial Virulence".
She is working as a Post Doctorate fellow in Dr. Igor Kramnik’s lab at NEIDL, Boston University. Her current project is focused on understanding the pathophysiology of granulomas formed during the progression of TB infection at molecular and cellular level.