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Related Concept Videos

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Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Neuroinflammatory Consequences of Rhinovirus Infection in Human Epithelial and Neuronal Models.

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Rhinovirus directly infects airway nerves, triggering inflammation and heightened TRPA1 channel sensitivity. This suggests a mechanism for virus-induced cough in lung disease exacerbations.

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Area of Science:

  • Neuroscience
  • Immunology
  • Respiratory Medicine

Background:

  • Rhinovirus (RV) is a primary cause of lung disease exacerbations.
  • Airway sensory nerves' role in RV-induced symptoms is not fully understood.
  • A novel peripheral neuronal equivalent (PNE) model derived from stem cells was utilized.

Purpose of the Study:

  • To investigate the direct effects of RV infection on airway sensory nerves (PNEs).
  • To determine if RV alters PNEs directly or indirectly through epithelial cell mediators.
  • To explore the role of IL-1β in RV-induced neuronal responses.

Main Methods:

  • RV-A16 infection of PNEs and primary bronchial epithelial cells (PBECs).
  • Confirmation of viral replication via titration, immunofluorescence, and western blotting.
  • Transcriptomic analysis (RNA sequencing) and inflammatory profiling; calcium imaging to assess TRPA1 channel activity.

Main Results:

  • RV-A16 successfully infected and replicated in both PNEs and PBECs.
  • Upregulation of gene signatures related to antiviral response, sensory neuropathy, and NMDA receptor activity in PNEs.
  • Increased IL-1β release from infected cells, leading to heightened PNE TRPA1 channel sensitivity.

Conclusions:

  • The PNE model is suitable for studying direct RV effects on airway nerves.
  • RV-induced IL-1β release from epithelium enhances neuronal TRPA1 responses.
  • This pathway offers a potential mechanism for virus-induced cough hypersensitivity in lung diseases.