Abstract

Information about the spectrum of disease caused by hepatitis E virus (HEV) genotype 3 is emerging. During 2004–2009, at 2 hospitals in the United Kingdom and France, among 126 patients with locally acquired acute and chronic HEV genotype 3 infection, neurologic complications developed in 7 (5.5%): inflammatory polyradiculopathy (n = 3), Guillain-Barré syndrome (n = 1), bilateral brachial neuritis (n = 1), encephalitis (n = 1), and ataxia/proximal myopathy (n = 1). Three cases occurred in nonimmunocompromised patients with acute HEV infection, and 4 were in immunocompromised patients with chronic HEV infection. HEV RNA was detected in cerebrospinal fluid of all 4 patients with chronic HEV infection but not in that of 2 patients with acute HEV infection. Neurologic outcomes were complete resolution (n = 3), improvement with residual neurologic deficit (n = 3), and no improvement (n = 1). Neurologic disorders are an emerging extrahepatic manifestation of HEV infection.

Highlights

  • The association between neurologic signs and symptoms and hepatitis E virus (HEV) infection has been based on detection of anti-HEV immunoglobulin (Ig) M in serum

  • From January 2005 through December 2009, in the Department of Hepatology of Toulouse University Hospital, among 21 patients with acute HEV infection, neurologic signs and symptoms developed in 1 (4.76%). We describe these 7 cases of HEV-induced neurologic disorders, which occurred in 3 nonimmunocompromised patients with acute HEV infection, in 2 kidney transplant recipients and 1 kidney–pancreas transplant recipient with chronic HEV infection, and in 1 HIV-positive patient with chronic HEV infection (Tables 1, 2)

  • Data about neurologic sequelae of HEV infection are scarce and come mainly from the Indian subcontinent. These data probably refer to HEV genotype 1 infection because this is the predominant genotype in this area

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Summary

Introduction

The association between neurologic signs and symptoms and HEV infection has been based on detection of anti-HEV immunoglobulin (Ig) M in serum. From January 2004 through April 2009, in the organ-transplant unit of Toulouse University Hospital, among 50 solid-organ–transplant patients with HEV, neurologic signs and symptoms developed among 3 (6%). From January 2005 through December 2009, in the Department of Hepatology of Toulouse University Hospital, among 21 patients with acute HEV infection, neurologic signs and symptoms developed in 1 (4.76%). We describe these 7 cases of HEV-induced neurologic disorders, which occurred in 3 nonimmunocompromised patients with acute HEV infection, in 2 kidney transplant recipients and 1 kidney–pancreas transplant recipient with chronic HEV infection, and in 1 HIV-positive patient with chronic HEV infection (Tables 1, 2)

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