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Updated: Feb 4, 2026

In Vitro Analysis of Myd88-mediated Cellular Immune Response to West Nile Virus Mutant Strain Infection
Published on: November 27, 2014
West Nile Virus as a Trigger for Acute Inflammatory Demyelinating Polyneuropathy: Exploring Intravenous
Matthew D Howard1, Justin Baman2, Ramsha Bhutta3
1Internal Medicine, St. Francis Hospital, Columbus, USA.
Abstract:
West Nile virus (WNV) is a rare trigger of acute inflammatory demyelinating polyneuropathy (AIDP), more commonly associated with meningoencephalitis. This case highlights an atypical post-infectious presentation of WNV-associated AIDP following recent viral illness and explores the associated diagnostic and therapeutic challenges. A 36-year-old male patient with heavy alcohol use, chronic tobacco exposure, and a recent upper respiratory infection developed rapidly progressive bilateral weakness, numbness, and paresthesias over several days, ultimately becoming unable to walk. Examination revealed areflexia, distal-predominant sensory loss, ataxia, and cerebellar tremor. Cerebrospinal fluid analysis showed albuminocytologic dissociation, and serologic testing was positive for WNV immunoglobulin M (IgM) and immunoglobulin G (IgG), suggesting recent or ongoing infection. Electrodiagnostic studies demonstrated a mixed demyelinating and axonal polyneuropathy with secondary axonal loss. Brain MRI revealed a small, nonspecific focus of possible demyelination, while spine MRI showed no nerve root enhancement. The patient was treated with a standard five-day course of intravenous immunoglobulin (IVIG) with respiratory monitoring and supportive care, resulting in gradual strength improvement and eventual restoration of functional mobility. This case emphasizes the diagnostic complexity of distinguishing WNV-associated AIDP from other neuroinvasive or immune-mediated neurologic conditions and underscores the importance of early recognition and timely immunotherapy. In addition, the patient's significant alcohol and tobacco exposure highlights the potential influence of comorbid substance use on immune function and recovery trajectory. Although our patient experienced favorable improvement with standard therapy, prior reports suggest potential variability in IVIG responsiveness among WNV-associated neuropathies, representing an important area for further investigation.
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