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Aftab Ansari, Ph.D.

Pathology and Laboratory Medicine

  • Ph.D., University of Arizona, Tucson, Arizona, 1970
  • M.S., University of California, Los Angeles, CA, 1967
  • M.S., University of Karachi, Karachi, Pakistan, 1963
  • B.S., University of Karachi, Karachi, Pakistan, 1961
Phone: (404) 712-2834
Address: 2309 WMB Bldg.
Email: pathaaa@emory.edu

Research Interests: Our lab research utilizes SIV infected disease susceptible Asian rhesus macaques ( RM ) and SIV infected disease resistant African sooty mangabeys ( SM ) to delineate cellular and molecular mechanisms by which SIV infection of these two species results in such distinct clinical outcomes. Research includes a) characterization of methods to protect the SIV infected RM from developing disease with the use of recombinant RM cytokines which thus includes PCR assisted cloning, sequencing and preparation of RM interleukins 2, 4, 12, 15 etc, and optimizing their use in vivo b) methodologies to achieve immune reconstitution with the use of autologous cell based therapies which involves isolation of CD4+ T cells from the monkeys prior to and or post SIV infection, expanding these in vitro and then infusing them into the autologous monkeys under the umbrella of ant-viral chemotherapy in efforts to establish feasibility to perform similar therapies in HIV infected humans c) studies of the role of mast cells as reservoirs of viral infection which involves delineation of the mode of entry and mechanisms of viral latency and breakdown in this cell lineage with the use of Toll like receptor ligands and the use of the SCID-HU-rag-IL-2R -/-,hu-SCF Tg mice as recipients of this cell lineage d) delineation of differences in the intracellular signaling cascades within CD4+ T cells from SIV infected as compared to uninfected RM and SM, studies which are currently focused on unraveling signaling molecules involved in the regulation of the cell cycle e) delineation of the differences in the host proteins that become an integral part of the virus as it is assembled and egresses out of CD4+ T cells and macrophages from the disease susceptible and disease resistant RM and SM, respectively. It is reasoned that results of the studies outlined above will provide insights into the mechanisms of disease susceptibility and resistance which can then be utilized to formulate therapeutic strategies for human HIV infection.