Henry Godfrey
Academic Editor

Henry P. Godfrey


Professor of Pathology, New York Medical College.

Fellow, American Academy of Microbiology, New York Academy of Medicine.

Member, American Association of Immunologists, British Society for Immunology, American Society for Microbiology, New York Academy of Sciences, American Association for Science, Harvey Society.

Allergy & Clinical Immunology Immunology Infectious Diseases Microbiology Pathology

Institution affiliations

Work details

Professor of Pathology

New York Medical College
June 1982
Department of Pathology
Tuberculosis is a global public health problem, and the second most common cause of death of adults from infectious disease throughout the world (AIDS is number one). Roughly a third of the world's population is infected with Mycobacterium tuberculosis. The recent increase in the incidence of tuberculosis world-wide as a result of the HIV epidemic has led to increased interest in cellular immunity and pathogenesis in this disease. From my initial focus on biochemical mechanisms of delayed-type hypersensitivity in tuberculosis and the role of a specialized fibronectin, T cell fibronectin, in mediating this immune response, our emphasis has expanded over the years to include examination of the role of secreted mycobacterial proteins such as the fibronectin-binding antigen 85 proteins in the pathogenesis of tuberculosis, development of diagnostic reagents for active mycobacterial infection in human beings and domestic animals, as well as in captive and free-ranging wild animals that are not dependent on host immune response, delineation of a putative regulatory sequence in the mycobacterial genome and investigation of the role of interactions between mycobacterial DNA and eukaryotic transcription factors and nuclear proteins in the pathogenesis of tuberculosis. In collaboration with Dr. Felipe Cabello of the Department of Microbiology and Immunology here at New York Medical College, we have been actively involved in analyzing the regulation of expression of a family of basic surface membrane proteins (BmpA, BmpB, BmpC, BmpD) of Borrelia burgdorferi, the spirochete that causes of Lyme disease. We have also collaborated with Dr. Cabello on developing new genetic and immunochemical tools for studying B. burgdorferi in order to analyze the genes and gene products involved in the pathogenesis of Lyme disease. Despite our current interests in pathogenesis of infectious disease, we still retain a strong intellectual interest in the biochemical mechanisms underlying delayed hypersensitivity and contact dermatitis in human beings and animals. This has resulted in several on-going collaborative studies in this area with a number of scientists across the United States.


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