Theresa L. Chang

Biography

Dr. Theresa Chang has been working on the molecular basis of virus-host interactions since she was a Ph.D student in Dr. Alice's Huang's Laboratory at NYU where she demonstrated the differential regulation of Vesicular Stomatitis Virus RNA transcription and replication by viral NS protein via cellular phosphatase. During her postdoctoral trainings at Yale University with Joan Steitz and Xin-Yuan Fu, she discovered that IL-4 blocked tumor cell proliferation through STAT1 activation. In Dr. John Moore’s laboratory, Dr. Chang demonstrated that that CD8 antiviral factors, found in long-term HIV-infected nonprogressors, inhibited HIV infection through STAT1 signaling pathway. Meanwhile, she discovered that RANTES, a ligand for CCR5 receptor, enhanced HIV infection by activation of MAP kinase through interaction with glycosaminoglycan. As a scientist at Osel, Inc. and a visiting scholar at Stanford University, she developed a co-culture system for bacteria and mammalian cells to demonstrate anti-HIV activity of a primary isolate of lactobacilli, commensal bacteria in the vaginal mucosa, engineered to express CD4. As a faulty at MSSM, she demonstrated the dual role of human alpha-defensin-1 (HNP for human neutrophil peptide) in anti-HIV immunity by acting on the virion and target cell. Similar to its anti-HIV effect on the target cell, HNP-1 inhibits influenza viral infection through suppression of PKC signaling pathway. Recently, my laboratory discovered human defensins 5 and 6 (HD5 and HD6), highly abundant in the gut and crucial for the control of bacteria pathogens, were induced in response to gonococcal (GC) infection in vitro and in the genital mucosa, resulting in an increase in HIV infectivity. We also found that GC infection enhanced HIV infection of resting CD4+ T cells through TLR2 activation.