Amy Y Vittor1, Maureen Long2, Paramita Chakrabarty3, Lauren Aycock4, Vidya Kollu1, Steven T DeKosky5. 1. Division of Infectious Disease and Global Medicine, University of Florida, Gainesville, FL, USA. 2. College of Veterinary Medicine, Department of Comparative, Diagnostic, and Population Medicine, University of Florida, Gainesville, FL, USA. 3. Department of Neuroscience, Center for Translational Research in Neurodegenerative Diseases, and McKnight Brain Institute, University of Florida, Gainesville, FL, USA. 4. School of Medicine, University of Florida, Gainesville, FL, USA. 5. Department of Neurology and McKnight Brain Institute, University of Florida, Gainesville, FL, USA.
Abstract
PURPOSE OF REVIEW: West Nile virus (WNV) emerged from Central Africa in the 1990s and is now endemic throughout much of the world. Twenty years after its introduction in the USA, it is becoming apparent that neurological impairments can persist for years following infection. Here, we review the epidemiological data in support of such long-term deficits and discuss possible mechanisms that drive these persistent manifestations. RECENT FINDINGS: Focusing on the recently discovered antimicrobial roles of amyloid and alpha-synuclein, we connect WNV late pathology to overlapping features encountered in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. We also summarize new research on microglial activation and engulfment of neural synapses seen in recovered WNV as well as in neurodegenerative diseases, and discuss how loss of integrity of the blood-brain barrier (BBB) may exacerbate this process. SUMMARY: Neuroinvasive viral infections such as WNV may be linked epidemiologically and mechanistically to neurodegeneration. This may open doors to therapeutic options for hitherto untreatable infectious sequelae; additionally, it may also shed light on the possible infectious etiologies of age-progressive neurodegenerative dementias.
PURPOSE OF REVIEW: West Nile virus (WNV) emerged from Central Africa in the 1990s and is now endemic throughout much of the world. Twenty years after its introduction in the USA, it is becoming apparent that neurological impairments can persist for years following infection. Here, we review the epidemiological data in support of such long-term deficits and discuss possible mechanisms that drive these persistent manifestations. RECENT FINDINGS: Focusing on the recently discovered antimicrobial roles of amyloid and alpha-synuclein, we connect WNV late pathology to overlapping features encountered in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. We also summarize new research on microglial activation and engulfment of neural synapses seen in recovered WNV as well as in neurodegenerative diseases, and discuss how loss of integrity of the blood-brain barrier (BBB) may exacerbate this process. SUMMARY: Neuroinvasive viral infections such as WNV may be linked epidemiologically and mechanistically to neurodegeneration. This may open doors to therapeutic options for hitherto untreatable infectious sequelae; additionally, it may also shed light on the possible infectious etiologies of age-progressive neurodegenerative dementias.
Entities:
Keywords:
Alpha-synuclein; Alzheimer’s disease; Amyloid beta; Antimicrobial peptide; Neurodegenerative disease; Neurological sequelae; Parkinson’s disease; West Nile virus
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