Rahm Gummuluru PhD
Associate Professor,
Department of Microbiology,
Boston University School of Medicine

Research in my laboratory is broadly focused on the mechanisms of cell-­to-­cell  and  cell-­associated  HIV-­1 transmission with an emphasis on interactions of HIV with myeloid cells (monocytes, macrophages, and dendritic cells) and the implications of these interactions on systemic dissemination of HIV. I obtained a Ph.D. at the University of Rochester in Rochester, NY where I studied mechanisms responsible for the rapid immunopathology and disease progression observed in SIVsmmPBj14-­infected  pig-­tailed  macaques.  As a post-­ doctoral fellow at the Fred Hutchinson Cancer Research Center in Seattle, I focused on HIV-­1 pathogenesis, with an emphasis on host interactions of the HIV-­1 accessory protein, Vpr and the mechanism by which Vpr enhances  HIV-­1  replication.  I  am now an Associate  Professor in the Department of Microbiology at Boston University School of Medicine (BUSM), and Co-­Director of the Developmental Core for the Lifespan/BU/BMC CFAR. My research has been focused on understanding the molecular mechanisms that govern interactions of HIV with myeloid cells. My laboratory has considerable expertise in molecular virology, identifying mechanisms of   HIV-­induced immunopathology and cell biology of HIV   infection. We were the first to identify the glycosphingolipid,   GM3, present in the virus particle membrane and the myeloid cell-­specific siglec, CD169/Siglec-­1, as the ligand-­receptor interaction necessary for capture of HIV-­1 particles by DCs,  and transfer of the captured virus particles to the myeloid cell-­mediated trans infection pathway across virological synapses. The discovery of the GM3 – CD169 mechanism of virus particle recognition by my laboratory has paved the way for our recent  efforts to develop nanoparticle-based myeloid  cell-­specific therapeutics for targeted delivery of  anti-­retrovirals to secondary lymphoid tissues.  In parallel,  we are focused on identifying mechanisms that drive persistent induction of innate immune activation in HIV-­infected myeloid cells, with the ultimate goal of developing immunotherapeutic approaches to diminish HIV-­induced chronic immune activation, the main driver of HANA conditions in cART-­suppressed individuals.