Victor Moyo graduated from the University of Zimbabwe School
of Medicine in 1991. Upon graduation, he took a position as a research
fellow with Victor Gordeuk M.D in Zambia in an NIH sponsored randomized
double blind placebo controlled clinical trial which looked at iron
chelation as an adjunct to quinine in the treatment of cerebral malaria
in children. After clinical training, he returned to the University
of Zimbawe and Dr. Gordeuk to work as a clinical research Fellow on
another NIH sponsored research project which sought to identify evidence
for genetic transmission of iron overload. At that time he developed
an interest in the role of cytokines in the infectious processes of
tuberculosis and HIV and the effect of immuno-modulation brought about
by environmental factors such as iron loading. He came to the United
States in 1996 and completed internship and residency at the George
Washington University in 1999 and is currently in training as a 3rd
year fellow in Hematology and Oncology at the Johns Hopkins University.
He is interested in the pathogenesis of endemic Burkitt’s lymphoma,
AIDS-associated lymphomas, and international public health. Otto Martinez-Mazza
and Kenrad Nelson served as his mentors.
Dr. Jonathan Schneck is a Professor of Pathology at Hopkins with an internationally known laboratory devoted to understanding antigen specific T cells in both normal physiologic immune responses as well as in several disease states. Adoptive immunotherapy has been impeded by the lack of an economical and reproducible method to generate therapeutic numbers of antigen-specific CTL. An artificial Antigen-Presenting Cell (aAPC), made by coupling HLA-Ig and anti-CD28 to beads, may serve as a platform that will enable the reliable induction and expansion of antigen-specific CTL. His preliminary data indicate that aAPC can induce and expand clinically relevant target T cell populations directed at CMV, (using the A2-restricted, immunodominant CMV peptide derived from pp65 viral antigen, NLVPMVATV) and at melanoma (using the A2-restricted, Mart-1 peptide, ELAGIGILTV). Furthermore, he has found that aAPC compare favorably with the “gold standard” dendritic cell-mediated expansion of antigen-specific CTL. Dr. Schneck’s interest in lymphoma stems from his recent studies on the development of aAPC for use in ex vivo expansion of antigen-specific CTL for immunotherapy. He hopes to investigate the use of aAPC in expansion of antigen specific cells in EBV-associated lymphomas initially and ultimately in lymphoma more generally as appropriate target antigens are identified. Dr. Schneck has worked closely with Drs. Ambinder and Levitsky in these efforts.
Dr. Andrea Cox is a post-doctoral and clinical fellow in the Division of Infectious Diseases at Johns Hopkins University. Her graduate work focused on identification of tumor antigens and she remains interested in the immune response to malignancies. As an infectious disease fellow working in the laboratories of Dr. Drew Pardoll and of Dr. David Thomas, she has been studying the immune response to hepatitis C virus (HCV) infection. Dr. Thomas is a leading expert in the epidemiology and natural history of HCV infection and studies several large cohorts of HCV infected individuals. Dr. Pardoll is a noted expert in tumor immunology. HCV infects approximately 1.7% of Americans and causes significant morbidity and mortality from cirrhosis, hepatocellular carcinoma, essential mixed cryoglobulinemia, and a variety of other extrahepatic manifestations. HCV is the stimulus for the apparent benign lymphoproliferative process underlying a wide spectrum of clinical features and is also hypothesized to play a role in the progression to frank lymphoid malignancy in a subgroup of patients. Current data indicate a higher prevalence of overt B-cell non-Hodgkin's lymphoma (NHL) in HCV-infected patients, especially in some geographic areas. In addition, the putative role of hepatitis C virus (HCV) infection in the pathophysiology of lymphoproliferative diseases is supported by north-American and south-European studies reporting HCV seroprevalence up to 32% in patients with idiopathic B-cell NHL. The frequency of NHL, however, is much lower than that of HCV infection, suggesting that HCV infection alone is not able to induce lymphoma and that other events are required to produce a malignant B cell phenotype. Stimuli created by the immune response to this chronic infection may be involved in the pathogenesis of NHL. Further studies are required to understand the mechanisms underlying this association. The combined expertise of the immunologists, oncologists, and HCV experts at Hopkins teamed with our ongoing studies of the immune response to HCV in well characterized, large cohorts of infected subjects followed regularly over years provide a rare opportunity to study the progression to lymphoma. Dr. Cox is enthusiastic about applying her experience with tumor immunology to the study of HCV and its relationship to NHL.