个人简介

Dr. Andrea L. Cox is a professor of medicine at the Johns Hopkins University School of Medicine and a member of the Johns Hopkins Kimmel Cancer Center. She holds joint appointments in oncology and, at the Johns Hopkins Bloomberg School of Public Health, in molecular microbiology and immunology. She is an internationally recognized leader in studies of the host immune response to chronic viral infections, including HIV, hepatitis B and hepatitis C (HCV). Dr. Cox serves as the director of the Medical Scientist Training Program. Dr. Cox earned her Ph.D. in chemistry from the University of Virginia, where she worked on the characterization of peptide T cell antigens. She then earned her M.D. and completed internal medicine residency and infectious disease fellowship training at Johns Hopkins. She leads the largest prospective cohort study of acute HCV infection designed to enable detailed molecular analysis of HCV transmission, host immune responses and virus sequence evolution. She is the principal investigator on the first prophylactic HCV vaccine trial in individuals at risk of HCV infection. In addition to her research on chronic viral infections, Dr. Cox is actively involved in clinical care of patients with HCV, HIV and hepatitis B infection. A teacher, advisor and mentor of physician-scientists, Dr. Cox is a faculty member in the cellular and molecular medicine and the immunology graduate programs at the School of Medicine. Dr. Cox also serves as the faculty advisor for the Association of Women Student MD-PhDs. MD, Johns Hopkins University School of Medicine (1998)

研究领域

Viral Immunology; Virus; Protective immunity; Hepatitis C virus; T cell; Vaccine; Immunotherapy

Dr. Cox’s laboratory investigates the host immune response to chronic human viral infections, particularly HIV and hepatitis C virus (HCV). HCV infects nearly 200 million people worldwide, resulting in chronic infection in about 75% of cases. They examine the role of the immune response in clearance of HCV upon exposure to this virus by studying responses to HCV from the earliest phases of infection through years following infection in a longitudinal, prospective cohort of people at risk of HCV infection. This allows a comparison of the innate, humoral and cellular immune responses to infection with clearance versus persistence. They have demonstrated that spontaneous control of HCV does not uniformly generate sterilizing immunity, but reinfection is associated with a reduction in the magnitude and duration of viremia (compared with the initial infection), broadened cellular immune responses and generation of cross-reactive humoral responses. These findings are consistent with development of adaptive immunity that is not sterilizing but protects against chronic disease. To identify mechanisms of protective immunity against HCV infection and improve prophylactic HCV vaccine design, they are determining the cellular and humoral responses associated with repeated HCV control. A significant barrier to the development of an HCV vaccine is that HCV is a highly diverse virus. The laboratory has also developed and evaluated methods of HCV vaccine design that may overcome this diversity and stimulate an effective immune response.

近期论文

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Cox A, Mosbruger T, Mao Q, Liu Z, Wang X-H, Yang H-C, Sidney J, Sette A, Pardoll D, Thomas D, Ray R.; Cellular Immune Selection with Hepatitis C Virus Persistence in Humans, The Journal of Experimental Medicine 2005 201: 1741-1752. Osburn W, Fisher B., Dowd K, Urban G, Liu L, Ray S, Thomas D, and Cox A. Spontaneous control of primary hepatitis C virus infection and immunity against persistent reinfection. Gastroenterology 2010 Jan; 138(1):315-24. Chattergoon M, Latanich R, Quinn J, Winter M, Buckheit R, Blankson J, Pardoll D, Cox AL., HIV and HCV activate the inflammasome in monocytes and macrophages via endosomal Toll-like receptors without induction of Type 1 interferon. PLoS Pathogens 2014 May 01;10(5): e1004082 Veenhuis RT, Astemborski J, Chattergoon MA, Greenwood P, Jarosinski M, Moore RD, Mehta SH, Cox AL, Systemic Elevation of Proinflammatory Interleukin 18 in HIV/HCV Coinfection versus HIV or HCV Monoinfection. Clinical Infectious Diseases 2017, 64 (5): 589-596. Park BV, Freeman ZT, Ghasemzadeh A, Chattergoon MA, Rutebemberwa A, Steigner J, Winter ME, Huynh TV, Sebald SM, Lee SJ, Pan F, Pardoll DM, Cox AL. TGF-β1-Mediated Smad3 Enhances PD-1 Expression on Antigen-Specific T Cells in Cancer. Cancer Discovery. 2016 Dec;6(12):1366-1381. Cox AL. Global Control of Hepatitis C Virus. Science 2015 August 21: 349 (6250):790-1.