Hepatitis E virus‐associated Guillain–Barre syndrome: Revision of the literature

The association between preceding infection of hepatitis E virus (HEV) and Guillain–Barre syndrome (GBS) has been found for more than a decade, while hepatitis E virus‐associated Guillain–Barre syndrome (HEV‐associated GBS) still remains poorly understood. Initially discovered in 2000, the association between GBS and HEV has been focused by neurologists increasingly. Five percent of patients with GBS had preceding acute HEV infection in the Netherlands and higher rate was found in Bangladesh (11%) where HEV is endemic. Method An extensive review of relevant literature was undertaken. Results Hepatitis E virus infection may induce GBS via direct viral damage according to recent research findings. On the other hand, the presence of antiganglioside GM1 or GM2 antibodies in serum of some HEV‐associated GBS patients indicates that HEV infection may trigger GBS by activating autoimmune response to destroy myelin or axon mistakenly. Management of HEV‐associated GBS has no obvious difference from GBS. It mainly consists of supportive therapy and immunotherapy. Intravenous immunoglobulin (IVIG) or plasma exchange (PLEX) was used in most reported cases, which is the main strategy for clinical treatment of HEV‐associated GBS. Whether antiviral therapy could be additional strategy other than the routine therapy to shorten the length of disease course is one of the most urgent problems and requires further study. Conclusions An overview of possible pathogenesis will gain a first insight into why HEV, traditionally recognized as only hepatotropic, can induce many neurological disorders represented by GBS. Moreover, understanding of the underlying mechanisms may contribute to development of a novel therapeutic strategy. This review also summarizes management and clinical characteristics of HEV‐associated GBS, aiming to achieve early recognition and good recovery.