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Poonia Bhawna
Assistant Professor
Division of Basic Science and Vaccine Research
IHV, University of Maryland
Baltimore
USA
After obtaining DVM and PhD degrees,she worked as research scientist with a focus on viral infectious diseases and therapy. At Cornell University, she designed tools for identification and molecular characterization of new viral pathogens of poultry and identified a new strain of virus circulating in poultry in USA. Her research identified mechanisms of tumor induction by Marek’s Disease Virus, immune responses relevant against tumors and potential vaccine targets. Afterwards, led projects on AIDS pathogenesis and my research identified potential HIV target cells in vagina using immunohistochemistry, confocal microscopy and flow cytometry, and identified immune factors affecting HIV transmission. Currently, her research explores effective vaccine development strategies against HIV and cancers using immunology, molecular biology and bioinformatics methods. A major focus is on examining ways to enhance natural and antibody mediated effector function of immune cells including natural killer cells and gamma delta T cells for improving therapy against diseases including HIV.
My research aims to identify means for improving vaccine-induced immune responses in HIV infection based on mechanisms of viral immunopathology. I have expertise in studying HIV pathogenesis including mucosal SIV infection in rhesus macaques, SIV vaccine immune responses, FcR-antibody interactions and their significance in HIV disease. I am currently investigating the cytotoxic CD8 T cell subsets relevant for controlling HIV infection using cohorts of HIV infected individuals who progress to disease in absence of therapy or those who control the infection spontaneously. Another area of research focus is immune activation caused by FcgR signaling and it’s consequence on the balance between HIV replication and anti-HIV effector function. We found that functional polymorphisms in FCgR genes are associated with HIV transmission and progression and there is potential for exploiting FcGR expressing gamma/delta T cells as effectors for antibody-dependent cellular cytotoxicity in HIV+ patients.
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