Associate Professor

Lewis Hall, #3186
Office: (757) 446-5174
Lab: (757) 446-7122
Fax: (757) 446-7426
Email: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Teaching: Bioinformatics (Course Director), Biostatistics for Biomedical Sciences (Course Director), Concepts in Cell Biology and Physiology, Concepts in Research Design, Medical Microbiology and Immunology (MMI), Medical Master Library Research Thesis, Applied Biotechnology Internship

Biomedical Sciences Program Tracks: Molecular Integrative Biosciences (MIB), Molecular and Cellular Biology

Education

• B.A., Biology, Bard College, Annandale-on-Hudson, NY
• Ph.D., Cellular and Molecular Biology, University of Wisconsin, Madison, WI
• Postdoctoral Training, COH/Beckman Research Institute, Duarte, CA

Research Interests

Dr. Lundberg's laboratory works on the immune response to the agent behind common cold sores, herpes simplex virus 1 (HSV-1). HSV-1 is a neurotropic pathogen that, as part of the normal course of infection, enters into a dormant state in the infected neuron. When disturbed through stress (sunburn, physical, mental), HSV-1 can reactivate. This is why patients almost always experience cold sores in the same location; that is, where the infected neuron connects to the skin surface. However, there are several areas of human HSV-1 related disease with the potential for much more dire consequences than an irritating blister.

When HSV-1 infects the cornea (and subsequently, the brain), the pathology that results is directly tied to the quality of the immune response during acute infection. In the case of sensitive tissues, such as the eye and the central nervous system (CNS), this means an immune response of appropriate strength under suitable control to avoid “collateral” damage.

Unfortunately, some patients still suffer the consequences of an overly exuberant inflammatory response during HSV-1 infection at these sites. Current focus is on the role of macrophages in the acute inflammation that develops within the CNS of susceptible individuals during HSV-1 infection. To do this, Dr. Lundberg's lab uses a mouse infection model to study very early changes in gene expression in the CNS and uses this information to understand why severe pathology develops in some strains of mice while others can control the infection without significant tissue destruction.

Selected Publications

                  Lundberg, P., H. J. Yang, S. J. Jung, M. A. Behlke, S. D. Rose, and E. M. Cantin. 2011. Protection against TNFalpha-dependent liver toxicity by intraperitoneal liposome delivered DsiRNA targeting TNFalpha in vivo. J Control Release (DOI:10.1016/j.jconrel.2011.10.034).

                  Sanders, M. S., G. T. van Well, S. Ouburg, P. S. Lundberg, A. M. van Furth, and S. A. Morre. 2011. Single nucleotide polymorphisms in TLR9 are highly associated with susceptibility to bacterial meningitis in children. Clin Infect Dis 52:475-480.

                  Ouburg, S., J. M. Lyons, J. A. Land, J. E. den Hartog, J. S. Fennema, H. J. de Vries, C. A. Bruggeman, J. I. Ito, A. S. Pena, P. S. Lundberg, and S. A. Morre. 2009. TLR9 KO mice, haplotypes and CPG indices in Chlamydia trachomatis infection. Drugs Today (Barc) 45 Suppl B:83-93.

                  Lundberg, P., C. Ramakrishna, J. Brown, J. M. Tyszka, M. Hamamura, D. R. Hinton, S. Kovats, O. Nalcioglu, K. Weinberg, H. Openshaw, and E. M. Cantin. 2008. The immune response to herpes simplex virus type 1 infection in susceptible mice is a major cause of central nervous system pathology resulting in fatal encephalitis. J Virol 82:7078-7088.

                  Lundberg, P., H. Openshaw, M. Wang, H. J. Yang, and E. Cantin. 2007. Effects of CXCR3 signaling on development of fatal encephalitis and corneal and periocular skin disease in HSV-infected mice are mouse-strain dependent. Invest Ophthalmol Vis Sci 48:4162-4170.

                  Lundberg, P., P. V. Welander, C. K. Edwards, 3rd, N. van Rooijen, and E. Cantin. 2007. Tumor necrosis factor (TNF) protects resistant C57BL/6 mice against herpes simplex virus-induced encephalitis independently of signaling via TNF receptor 1 or 2. J Virol 81:1451-1460.

                  Amarzguioui, M., P. Lundberg, E. Cantin, J. Hagstrom, M. A. Behlke, and J. J. Rossi. 2006. Rational design and in vitro and in vivo delivery of Dicer substrate siRNA. Nat. Protocols 1:508-517.

                  Kim, D. H., M. Longo, Y. Han, P. Lundberg, E. Cantin, and J. J. Rossi. 2004. Interferon induction by siRNAs and ssRNAs synthesized by phage polymerase. Nat Biotechnol 22:321-325.

                  Lundberg, P., and E. Cantin. 2003. A potential role for CXCR3 chemokines in the response to ocular HSV infection. Curr Eye Res 26:137-150.

                  Lundberg, P., P. Welander, X. Han, and E. Cantin. 2003. Herpes Simplex Virus Type 1 DNA Is Immunostimulatory In Vitro and In Vivo. J. Virol. 77:11158-11169.

                  Lundberg, P., P. Welander, H. Openshaw, C. Nalbandian, C. Edwards, L. Moldawer, and E. Cantin. 2003. A locus on mouse chromosome 6 that determines resistance to herpes simplex virus also influences reactivation, while an unlinked locus augments resistance of female mice. J Virol 77:11661-11673.

Return to the Department's Main Page