Training:
• B.A., 1968, Utah State University
• M.S., 1970, Utah State University
• Ph.D., 1974, University of Wisconsin
• Postdoctoral, 1975, University of Wisconsin Description and summary of research focus of the laboratory:
Dr. Larsen's laboratory desires to understand the genetics and control of disease for Chlamydiae. C. trachomatis, by itself, causes some 5 million cases of sexually transmitted disease in our country and 500 million in the world each year. Many of these lead to cervicitis, pelvic inflammatory disease and salpingitis, the latter of which has a high correlation with female infertility of the fallopian tubes. One goal is to understand the interaction of this obligate, intracellular parasite with its host to include means to interfere with the infectious process. Part of this process must be directed to a better understanding of the bacterium's genetics. So far some 350 of an expected 1000 genes have been identified in this attempt. Others need to be identified and functionality confirmed. Chlamydiaehave a number of interesting properties: They lack a peptidoglycan (PG) cell wall structure which is the rule in nearly all other bacteria: they cannot produce their own ATP but have some as yet unexplained mechanism for tapping host sources of ATP; they can prevent fusion with host-cell phagosomes--allowing their survival inside human cells--including macrophages; they have a developmental cycle which is also unusual in prokaryotes. We are interested in all of these functions. It is surprising that the first 8 genes for PG biosynthesis are present! What are the functions of the products of these 8 genes? On the other hand, a number of genes that are supposed to be present in Chlamydiae are not found. How do the bacteria make up for these apparent short-comings? How can we make a vaccine that will induce protection? What host factors will be required for protection from infection? How can we use our knowledge of these genes, including recA to develop a genetic system for chlamydial gene transfer? Elucidation of these chlamydia-specific characteristics will aid the understanding of its unique niche in life and ways to attack it. Publications
Welch, D., C-H. Lee, and S.H. Larsen (1990), Chlamydia trachomatis plasmid DNA detection with a two-step polymerase chain reaction. Appl. Environ. Microbiol., 56, 2494-2498. Hintz, N.J., D. Ennis, W.F. Liu and S.H. Larsen. (1995); The recA gene of Chlamydia trachomatis: Cloning, sequence, and characterization in Escherichia coli. FEMS Microbiol. Letters 127, 175-180. Jin, N., N. Hatton, D.R. Swartz, X. Xia, M.A. Harrington, S.H. Larsen, and R.A. Rhoades. (2000); Hypoxia activates JNK, ERK and p38 kinase in pulmonary arteries. Am. J. Respir. Cell & Mol. Biol. 23, 593-601. Jin, N., N. Hatton, M.A. Harrington, X. Xia, S.H. Larsen, and R.A. Rhoades. (2000); "H 2 O 2 -induced egr-1 and fra-1 gene expression is mediated by tyrosine kinase. Free Radical Biol. & Med. 29, 736-746. Zhong, Li, W. Li, Z. Yang, N. Maina, K. Qing, Y. Li, L. Chen, M. Tan, R. J. Chan, W. Zhao, S.H. Larsen, M. Yoder, W. Shou, A. Srivastava. (2004); Impaired nuclear transport and uncoating limit recombinant adeno-associated virus 2 vector-mediated transduction of primary murine hematopoietic cells, Human Gene Therapy. Search Pub Med Return to Homepage
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