 Patric S. J. Lundberg,
Ph.D.
Assistant Professor
Lewis Hall, #3186
Office: (757) 446-5174
Lab: (757) 446-7122
Fax: (757) 446-7426
Email: lundbeps@evms.edu
Teaching: Bioinformatics (Course Director)
Biomedical Sciences Program Tracks:
Molecular Integrative Biosciences (MIB); Molecular and Cellular
Biology
Education
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B.A., Biology, Bard College,
Annandale-on-Hudson, NY
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Ph.D., Cellular and Molecular Biology,
University of Wisconsin, Madison, WI
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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 (or 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. Currently, my 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 use 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
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Lundberg, P., H. Openshaw, M.
Wang, H.-J. Yang and E. Cantin (2007) Effects of CXCR3
Signaling on Development of Fatal Encephalitis, Corneal and Periocular
Skin Disease in HSV-1 Infected Mice is Mouse Strain
Dependent. IOVS, 48(9):
4162-4170.
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Lundberg, P., P. V. Welander, C.
K. Edwards, N. V. Rooijen, and E. Cantin. (2007) Tumor Necrosis
Factor (TNF) Protects Resistant C57BL/6 Mice Against Herpes Simplex
Virus-Induced Encephalitis Independently of Signaling Via TNFR1 or
TNFR2. J. Virol., 81(3):
p.1451-60.
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Amarzguioui, M.,
Lundberg, P., Cantin E.,
Hagstrom, J., Behlke, M. and Rossi, J.J (2006) Rational design and
in vitro/in vivo delivery of Dicer substrate siRNAs. Nature Protocols 1(2): 508-517.
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Kim, D. -H., Longo, M., Han,
Y., Lundberg, P.,
Cantin, E and Rossi, J.J. (2004) Interferon induction by
siRNAs and ssRNAs synthesized by phage polymerase. Nature Biotech. 22(3): 321-325.
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Lundberg,
P., Welander, P., Openshaw, H., Edwards,
C. K., Nalbandian, C., Moldawer, L. and. Cantin, E. M. (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(21):
11661-11673.
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Lundberg,
P., Han, X., Welander, P. and Cantin, E.
(2003) Herpes Simplex Virus Type 1 DNA Is Immunostimulatory In vitro
And In vivo. J. Virol. 77(20):
11158-11169.
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Lundberg,
P. and E. M. Cantin. (2003) A
Potential Role For CXCR3 Chemokines In The Response To Ocular HSV
Infection. Curr. Eye Res. 26(3-4):
137-150.
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Han, X.,
Lundberg, P, Tanamachi, B, Openshaw, H,
Longmate , J and Cantin, E. (2001) Gender Influences HSV-1 Infection
In Normal And Interferon-Gamma Mutant Mice. J.
Virol. 75(6): 3048-3052.
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Lundberg,
P., Splitter GA. (2000) gd
T-Lymphocyte Cytotoxicity Against Envelope-Expressing Target Cells Is
Unique To The Alymphocytic State Of Bovine Leukemia Virus-Infection In The
Natural Host. J Virol. 74(18):
8299-8306.
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