W — West Nile Virus
West Nile virus (WNV) is a neurotropic flavivirus maintained in a mosquito–bird transmission cycle. Humans are incidental hosts. The viral genome encodes structural proteins and non-structural proteins that antagonize interferon responses.
Following mosquito inoculation, WNV replicates in dendritic cells and spreads via viremia. Most infections are asymptomatic; about 20% develop West Nile fever, and less than 1% develop neuroinvasive disease.
Neuroinvasion mechanisms include direct endothelial infection, cytokine-mediated blood–brain barrier permeability, and leukocyte trafficking. In the CNS, WNV infects neurons, particularly in the brainstem and spinal cord anterior horn, which can produce acute flaccid paralysis resembling poliomyelitis.
Host age and immune status strongly influence severity. Type I interferon responses are critical for early viral control.
Research investigates determinants of neurovirulence, long-term neurologic sequelae, and host genetic factors influencing susceptibility.
West Nile virus (WNV) is a neurotropic flavivirus maintained in a mosquito–bird transmission cycle. Humans are incidental hosts. The viral genome encodes structural proteins and non-structural proteins that antagonize interferon responses.
Following mosquito inoculation, WNV replicates in dendritic cells and spreads via viremia. Most infections are asymptomatic; about 20% develop West Nile fever, and less than 1% develop neuroinvasive disease.
Neuroinvasion mechanisms include direct endothelial infection, cytokine-mediated blood–brain barrier permeability, and leukocyte trafficking. In the CNS, WNV infects neurons, particularly in the brainstem and spinal cord anterior horn, which can produce acute flaccid paralysis resembling poliomyelitis.
Host age and immune status strongly influence severity. Type I interferon responses are critical for early viral control.
Research investigates determinants of neurovirulence, long-term neurologic sequelae, and host genetic factors influencing susceptibility.