Dr. Patricia Spear is the John Evans Professor Emerita of Microbiology-Immunology at the Feinberg School of Medicine of Northwestern University. She received her B.A. degree from Florida State University, in bacteriology, and her PhD degree from the University of Chicago in microbiology. After postdoctoral training in immunology at the Rockefeller University, she served on the faculty of the University of Chicago from 1973-1987. In 1987, Dr. Spear was appointed Professor and Chair of Microbiology-Immunology at the medical school of Northwestern University. She served as Chair until 2003, then retired and closed her lab in 2009. Dr. Spear?s research focused on studies of herpes simplex virus entry into cells, including identification of cell surface receptors for viral entry, and investigation of the roles of multiple receptors in targeting the virus to critical cell types in disease (skin cells, nerve cells, immunocytes). The use of mouse mutants and mouse models of disease permitted demonstration that the mouse versions of human receptors identified in cultured cells are indeed critical for infection and disease. In addition to election to the National Academy of Sciences, Dr. Spear has been elected to the American Academy of Microbiology and the American Academy of Arts and Sciences.

Research Interests

I am interested in the mechanisms by which viruses invade cells, partricularly herpes simplex virus. Five of the viral envelope glycoproteins participate in viral entry into cells. We showed that the initial interaction of virus with cell is usually the binding of viral glycoproteins gB or gC to heparan sulfate chains on cell surface proteoglycans. In the years since, many other viruses and other microbes have been found to bind to heparan sulfate, a ubiquitous cell surface carbohydrate. Attachment of herpes simplex virus to heparan sulfate is not sufficient for entry. Entry requires the binding of a specific viral glycoprotein, gD, to any one of several different cell surface receptors, which we identified by expression cloning. The expression and distribution of these various gD receptors determine susceptibility of the cell to viral entry. Viral entry occurs by fusion of the viral envelope with the cell membrane. This fusion is triggered by the binding of gD to a gD receptor and requires the action of three other viral glycoproteins. Structure-function studies of the viral glycoproteins, entry receptors, and other cellular components will lead to an understanding of the mechanism of viral entry.

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Primary Section

Section 44: Microbial Biology

Secondary Section

Section 43: Immunology and Inflammation