U — Usutu Virus
Usutu virus (USUV) is a mosquito-borne flavivirus closely related to West Nile virus. Its single-stranded positive-sense RNA genome encodes a polyprotein cleaved into structural (C, prM/M, E) and nonstructural proteins (NS1–NS5). The E glycoprotein mediates receptor binding and membrane fusion.
USUV circulates primarily in a mosquito–bird enzootic cycle and has caused significant avian mortality in Europe. Humans are incidental hosts. Most human infections are asymptomatic or mild; however, neuroinvasive disease has been reported, particularly in immunocompromised individuals.
Pathogenesis involves viremia followed by possible neuroinvasion. As with other flaviviruses, blood–brain barrier disruption, infection of endothelial cells, and Trojan horse mechanisms via infected leukocytes may facilitate CNS entry. Within the brain, neuronal infection and microglial activation contribute to inflammation.
Innate immune responses, especially interferon signalling, are critical for viral control. Immunosuppression increases risk of severe disease.
Research focuses on viral emergence in temperate climates, cross-reactivity with other flaviviruses (which complicates serologic diagnosis), and determinants of neurovirulence. Climate change and vector expansion make USUV an emerging pathogen of interest in Europe.
Usutu virus (USUV) is a mosquito-borne flavivirus closely related to West Nile virus. Its single-stranded positive-sense RNA genome encodes a polyprotein cleaved into structural (C, prM/M, E) and nonstructural proteins (NS1–NS5). The E glycoprotein mediates receptor binding and membrane fusion.
USUV circulates primarily in a mosquito–bird enzootic cycle and has caused significant avian mortality in Europe. Humans are incidental hosts. Most human infections are asymptomatic or mild; however, neuroinvasive disease has been reported, particularly in immunocompromised individuals.
Pathogenesis involves viremia followed by possible neuroinvasion. As with other flaviviruses, blood–brain barrier disruption, infection of endothelial cells, and Trojan horse mechanisms via infected leukocytes may facilitate CNS entry. Within the brain, neuronal infection and microglial activation contribute to inflammation.
Innate immune responses, especially interferon signalling, are critical for viral control. Immunosuppression increases risk of severe disease.
Research focuses on viral emergence in temperate climates, cross-reactivity with other flaviviruses (which complicates serologic diagnosis), and determinants of neurovirulence. Climate change and vector expansion make USUV an emerging pathogen of interest in Europe.