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Academia Mexicana de Neurología, A.C.

2005, Number 5

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Rev Mex Neuroci 2005; 6 (5)

Molecular mimicry in Guillain-Barré syndrome’s neuropathogenesis

Ortega-Martínez MG, Jaramillo-Rangel G, Ancer-Rodríguez J, Trujillo JR

Language: Spanish
References: 60
Page: 440-447
PDF size: 91.66 Kb.


ABSTRACT

Guillain-Barré syndrome (GBS) is the most common autoimmune neuropathy. Clinically is characterized by an acute ascending flaccid paralysis that is often triggered by a preceding viral or bacterial infection. Campylobacter jejuni and cytomegalovirus (CMV) are the most frequent forebear pathogens. HIV-1 infection may be complicated by the GBS, which usually occurs prior to the development of AIDS. HIV-1 associated GBS has become a major problem and it is unclear whether the GBS ties to the HIV-1 virus itself or the reactivation to other viruses, such as CMV. Molecular mimicry between microbial and self-components is the mechanism that accounts for the humoral and cellular immune responses involved in the neuropathogenesis in GBS and others postinfectious autoimmune diseases. In this review we analyzed the role of molecular mimicry as the causative mechanism of GBS.


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