Virus infection of the Central Nervous System (CNS) can lead to damage to neurons and the development of neurological disease. Multiple cell types in the CNS are activated during virus infection and have important roles in regulating viral pathogenesis. The goal of our laboratory is to examine the interactions between the immune and nervous systems in regulating viral pathogenesis with the ultimate goal of identifying targets for therapeutic treatment of viral-mediated neurological diseases. We primarily utilize two different models of viral infections that mediate neuronal damage via either direct or indirect mechanisms. One model utilizes La Crosse Virus (LACV), a bunyavirus that is one of the leading causes of pediatric viral encephalitis in the United States. LACV induces neuronal apoptosis by directly infecting neurons. The other model of viral neuropathogenesis is a retrovirus model, where microglia and macrophages are the primary cell type infected in the CNS. In this model system, the damage to neurons is indirect. Our work with these viruses has identified mechanisms of both neuronal damage and neuronal protection that are mediated by specific interactions of the immune system with cells of the central nervous system. We are currently examining the regulation of these pathways and mechanisms in order to inhibit viral pathogenesis in the CNS.
Karin Peterson received her Ph.D. degree in microbiology and immunology in 1998 from the University of Missouri Medical School, where she studied autoimmunity and the activation of self-reactive T cells. She then went to Rocky Mountain Laboratories (RML) in 1998 as a postdoctoral fellow in the Laboratory of Persistent Viral Diseases and applied her skills in immunology toward understanding the mechanisms that control the immune response to retrovirus infection. During this time, she became interested in the immune responses to virus infections in the central nervous system (CNS). In 2004, Dr. Peterson accepted a position as an assistant professor at Louisiana State University School of Veterinary Medicine, where she furthered her studies on viral pathogenesis in the CNS and also taught classes in immunology and virology. In 2008, she returned to RML as a tenure-track investigator to study the innate immune responses in the CNS and their role in viral pathogenesis.
Taylor KG, Woods TA, Winkler CW, Carmody AB, Peterson KE Age-dependent myeloid dendritic cell responses mediate resistance to la crosse virus-induced neurological disease. J. Virol. 2014 Oct. 1; 88(19): 11070-9
Winkler CW, Taylor KG, Peterson KE. Location is everything: let-7b microRNA and TLR7 signaling results in a painful TRP. Sci Signal. 2014 May 27;7(327):pe14.
Christensen LB, Woods TA, Carmody AB, Caughey B, Peterson KE. Age-related differences in neuroinflammatory responses associated with a distinct profile of regulatory markers on neonatal microglia. J Neuroinflammation. 2014 Apr 4;11:70
Mukherjee P, Woods TA, Moore RA, Peterson KE. Activation of the innate signaling molecule MAVS by bunyavirus infection upregulates the adaptor protein SARM1, leading to neuronal death. Immunity. 2013 Apr 18;38(4):705-16.
Butchi NB, Woods T, Du M, Morgan TW, Peterson KE. TLR7 and TLR9 trigger distinct neuroinflammatory responses in the CNS. Am J Pathol. 2011 Aug;179(2):783-94.
Du M, Butchi NB, Woods T, Morgan TW, Peterson KE. Neuropeptide Y has a protective role during murine retrovirus-induced neurological disease. J Virol. 2010 Nov;84(21):11076-88.
Visit PubMed for a complete publication listing.
Last Updated October 01, 2014