Karin E. Peterson, Ph.D.

Senior Investigator

Neuroimmunology Unit

NIAID/DIR

Building 1, Room 1111
903 South 4th Street
Hamilton, MT 59840

406-375-9630

petersonka@niaid.nih.gov

Research Topics

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.

 

Credit: NIAID​SARM1 (red fluorescence) expression in the axons of neurons (stained with NeuN, green fluorescence) in brain tissue of La Crosse virus (LACV) infected mice. SARM1 was found to contribute to neuronal death following LACV infection both in vitro as well as

Figure 1: ​SARM1 was found to contribute to neuronal death following LACV infection both in vitro as well as in vivo (Mukherjee et.al. Immunity, 2013). Current studies are focused on examining the mechanism of SARM1-mediated neuronal damage.

Biography

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.

Selected Publications

  1. Winkler CW, Woods TA, Rosenke R, Scott DP, Best SM, Peterson KE. Sexual and Vertical Transmission of Zika Virus in anti-interferon receptor-treated Rag1-deficient mice. Sci Rep. 2017;7(1):7176.

  2. Winkler CW, Myers LM, Woods TA, Messer RJ, Carmody AB, McNally KL, Scott DP, Hasenkrug KJ, Best SM, Peterson KE. Adaptive Immune Responses to Zika Virus Are Important for Controlling Virus Infection and Preventing Infection in Brain and Testes. J Immunol. 2017;198(9):3526-3535.

  3. Mukherjee P, Winkler CW, Taylor KG, Woods TA, Nair V, Khan BA, Peterson KE. SARM1, Not MyD88, Mediates TLR7/TLR9-Induced Apoptosis in Neurons. J Immunol. 2015;195(10):4913-21.

  4. 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;38(4):705-16.

  5. Winkler CW, Race B, Phillips K, Peterson KE. Capillaries in the olfactory bulb but not the cortex are highly susceptible to virus-induced vascular leak and promote viral neuroinvasion. Acta Neuropathol. 2015;130(2):233-45.


This page was last updated on July 28th, 2017