The Landry-Guillain-Barré syndrome (LGBS) is a demyelinating disorder of the peripheral nervous system frequently preceded by infection with common viruses. Most prevalent among these agents are herpesviruses, particularly Epstein-Barr virus (EBV) and cytomegalovirus (CMV). The specific role played by antecedent viral infection in the pathogenesis of the LGBS remains obscure. In this regard, recent studies of Marek's disease (MD) neuropathy, an avian herpesvirus-induced experimental model for the LGBS, may provide insight. The autoimmune pattern of demyelination seen in MD neuropathy is histopathologically indistinguishable from that seen in the LGBS. In this paper, a comprehensive theory is discussed regarding the pathogenetic mechanisms that may be operative in the LGBS.