Title page for ETD etd-04032007-191751

Type of Document Master's Thesis
Author Lewis, Stephanie Diane
URN etd-04032007-191751
Title The Role of Toll-like Receptor 7 in the Neuropathogenesis of Retrovirus Infection in Neonates
Degree Master of Science (M.S.)
Department Pathobiological Sciences (Veterinary Medical Sciences)
Advisory Committee
Advisor Name Title
Karin Peterson Committee Chair
David Baker Committee Member
Stephania Cormier Committee Member
  • retrovirus
  • innate immune response
  • toll-like receptor
Date of Defense 2007-03-16
Availability unrestricted
Viral infections of the central nervous system (CNS) in infants are rare; however, they are associated with high morbidity and mortality rates. These virus infections often induce strong innate immune responses in the brain including: the production of cytokines and chemokines, the activation of astrocytes and microglia and the recruitment of macrophages. Innate immune responses are often initiated by toll-like receptors (TLR). Several studies have demonstrated that toll-like receptor 7 (TLR7) can be stimulated by single-stranded RNA from multiple viruses. In the current study, we examined the mechanism by which TLR7 contributes to neuroinflammation in the neonatal brain using a mouse model of polytropic retrovirus infection. We found that TLR7 deficiency had no effect on neurologic disease, viral replication, or induction of interferon beta mRNA. However, TLR7 deficiency significantly altered neuroinflammatory responses including proinflammatory cytokine production, astrocyte activation, and microglial/macrophage activation. To our knowledge, this is the first demonstration of the necessity of TLR7 for innate immune responses to retrovirus infection in vivo. Additionally, this indicates that the immune response to retrovirus in the CNS may not be essential for disease pathogenesis in neonates.
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