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Karin E. Peterson, Ph.D.
Rocky Mountain Laboratories
Bldg 1, Room 1111
903 South 4th Street
Hamilton, MT 59840
petersonka@niaid.nih.gov

Laboratory of Persistent Viral Diseases

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Karin E. Peterson, Ph.D.

Karin E. Peterson, Ph.D.

Chief, Neuroimmunology Unit, LPVD

Major Areas of Research

  • Examine how the innate immune response influences function of intrinsic brain cells during viral infections
  • Influence of the innate immune response on retrovirus infection and pathogenesis in the CNS
  • Influence of the innate immune response on bunyavirus infection and pathogenesis in the CNS
  • Examine autonomous and non-autonomous mechanisms of innate-immune induced neuronal damage/protection during viral infections of the CNS
 

Program Description

CNS Virus infection of the central nervous system (CNS) often results in damage to neurons and the development of neurological disease. Multiple cell types in the CNS are activated during virus infection and may play important roles in regulating viral pathogenesis. The goal of our laboratory is to determine how the innate immune responses of intrinsic brain cells such as astrocytes, microglia and neurons influence viral pathogenesis in the CNS with the ultimate goal of identifying targets for therapeutic treatment of viral-mediated neurological diseases. To examine the role of innate immune responses in the CNS, we utilize an indirect model of retroviral pathogenesis in the CNS. In this model, neurons are not directly infected but disease is induced through the activation of glial cells, reminiscent of what is observed with HIV infection in the CNS. We also examine the innate response of neurons to direct viral infection using La Crosse Virus (LACV), a bunyavirus which is one of the leading causes of pediatric viral encephalitis in the United States. Additionally, we are examining the direct effects of individual components of the innate immune response in triggering activation and damage of cells in the CNS using targeted activation of pattern recognition receptors in primary cultures of neuronal and glial cells.

Photo of neuropeptide Y expression
‚ÄčInduced expression of neuropeptide Y (red fluorescence) by neurons near virus-infected cells (green fluorescence) in the CNS following retroviral infection. Neuropeptide Y was shown to induce a protective response and slow the kinetics/onset of retroviral neuropathogenesis (Du, et.al. J. Virol., 2010).

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

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.

Mukherjee P, Butchi NB, Peterson KE. Pattern recognition receptor activation of intrinsic brain cells and influence on viral neurovirulence. In: Gemma C, ed. Neuroinflammation, pathogenesis, mechanisms and management. Haupage (NY): Nova Science Publishing; 2012. p. 245-71.

Du M, Butchi NB, Woods T, Peterson KE. Poly-thymidine oligonucleotides mediate activation of murine glial cells primarily through TLR7, not TLR8. PLoS One. 2011;6(7):e22454.

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.

Butchi NB, Du M, Peterson KE. Interactions between TLR7 and TLR9 agonists and receptors regulate innate immune responses by astrocytes and microglia. Glia. 2010 Apr 15;58(6):650-64.

Visit PubMed for a complete publication listing.

Last Updated June 13, 2013