College
Arts and Sciences
Student Level
Doctoral
Location
PAIS Building, Colloquium Room
Start Date
8-11-2021 4:00 PM
End Date
3-11-2021 5:00 PM
Abstract
Olfactory sensory neurons (OSNs) directly contact the environment and are exposed to pathogens, such as viruses. When OSNs detect a virus, they coordinate antiviral immune responses locally to stop virus progression into the brain, termed the central nervous system (CNS). For example, in COVID-19 patients the SARS-CoV-2 virus replicates in the olfactory epithelium resulting in loss of olfaction, yet viral detection in the CNS is rare. However, neuronal detection of a virus by OSNs will send electrical signals to the CNS via the olfactory bulb (OB) and shape our CNS. Because the OB is the nexus between the pathogen exposed olfactory epithelium and the vulnerable CNS, it is a hotspot for cooperation between neurons and immune cells. We previously identified a direct interaction between a virus and OSNs in rainbow trout, and reported antiviral immune responses in the OB, even without virus reaching to the OB. How neuronal signals trigger immune responses in the OB is not understood. The goal of this project is to understand how viral detection by OSNs mediates neuroimmune responses in a brain region, the OB. Preliminary data in a genetically pliable model, zebrafish, demonstrates viral-specific neuronal activation of OSNs projecting into the OB, suggesting that OSNs are electrically activated by viruses. Further, behavioral changes can be seen in both adult and larval zebrafish immediately after viral exposure. Cell identity and function can be inferred by looking at what genes are actively being expressed, or transcribed. By profiling the transcription of single cells in the OB after OSNs are exposed to virus, we found that both immune cells of the CNS, known as microglia, and neurons enter a protective state. This protective state is characterized by a decrease in gene expression of neuronal differentiation factors and an onset of innate immune response mediators. Thus, neurons in the OB appear to increase neuronal precursor status when a virus in detected in the olfactory epithelium. This study reveals how encounters with viruses in our nose throughout our lifetime may shape neuronal identity in our brains and result in behavioral responses in ways previously unrecognized.
Olfactory Detection of Viruses Shapes Brain Immunity and Behavior
PAIS Building, Colloquium Room
Olfactory sensory neurons (OSNs) directly contact the environment and are exposed to pathogens, such as viruses. When OSNs detect a virus, they coordinate antiviral immune responses locally to stop virus progression into the brain, termed the central nervous system (CNS). For example, in COVID-19 patients the SARS-CoV-2 virus replicates in the olfactory epithelium resulting in loss of olfaction, yet viral detection in the CNS is rare. However, neuronal detection of a virus by OSNs will send electrical signals to the CNS via the olfactory bulb (OB) and shape our CNS. Because the OB is the nexus between the pathogen exposed olfactory epithelium and the vulnerable CNS, it is a hotspot for cooperation between neurons and immune cells. We previously identified a direct interaction between a virus and OSNs in rainbow trout, and reported antiviral immune responses in the OB, even without virus reaching to the OB. How neuronal signals trigger immune responses in the OB is not understood. The goal of this project is to understand how viral detection by OSNs mediates neuroimmune responses in a brain region, the OB. Preliminary data in a genetically pliable model, zebrafish, demonstrates viral-specific neuronal activation of OSNs projecting into the OB, suggesting that OSNs are electrically activated by viruses. Further, behavioral changes can be seen in both adult and larval zebrafish immediately after viral exposure. Cell identity and function can be inferred by looking at what genes are actively being expressed, or transcribed. By profiling the transcription of single cells in the OB after OSNs are exposed to virus, we found that both immune cells of the CNS, known as microglia, and neurons enter a protective state. This protective state is characterized by a decrease in gene expression of neuronal differentiation factors and an onset of innate immune response mediators. Thus, neurons in the OB appear to increase neuronal precursor status when a virus in detected in the olfactory epithelium. This study reveals how encounters with viruses in our nose throughout our lifetime may shape neuronal identity in our brains and result in behavioral responses in ways previously unrecognized.
