Neuromuscular manifestations of human West Nile virus infection

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Opinion statement

Physicians in areas with active West Nile virus (WNV) transmission should be aware that WNV infection can present as a polio-like syndrome and that the spectrum of neuromuscular signs and symptoms may range from acute flaccid paralysis in the absence of fever or meningoencephalitis to subjective weakness and disabling fatigue. This awareness will help to avoid less tenable diagnoses and the morbidity associated with inappropriate treatment. Although anterior horns are the major site of spinal cord pathology, inflammatory changes also may involve spinal sympathetic neurons and ganglia, providing an explanation for the autonomic instability seen in some patients with WNV infection. However, the role that autonomic dysfunction plays in the morbidity and mortality of human WNV infection has to be elucidated. Another unresolved issue with important neuromuscular implications is whether WNV infection may lead to autoimmune disease. Support for this contention arises from reports of WNV patients presenting with various neuromuscular diseases that have a presumed autoimmune mechanism, including Guillain-Barré syndrome, other demyelinating neuropathies, myasthenia gravis, brachial plexopathies, and stiff-person syndrome. Although there is no specific treatment or vaccine currently approved for WNV infection in humans, and the standard is supportive care only, several drugs that can alter the cascade of immunobiochemical events leading to neuronal death may be potentially useful. Among these agents, minocycline (a semisynthetic derivative of tetracycline), interferon alpha, and high-dose corticosteroids are candidate therapies, although human experience is limited. In addition, passive immunization with intravenous immune globulin containing WNV-specific antibodies seems promising, based on anecdotal human reports.