Assuntos
Encéfalo/virologia , Vírus da Raiva/isolamento & purificação , Raiva/diagnóstico , Animais , Encéfalo/patologia , Técnicas e Procedimentos Diagnósticos , Modelos Animais de Doenças , Cães , Humanos , Mudanças Depois da Morte , RNA Viral/análise , Vírus da Raiva/genética , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
Two distinct clinical patterns, encephalitic (furious) and paralytic (dumb), have been recognized in human rabies. It has been postulated that different rabies virus variants associated with particular vectors may be responsible for these different clinical manifestations. Analysis of the glycoprotein (G), nucleoprotein (N), and phosphoprotein (P) genes of rabies viruses from 2 human cases of encephalitic rabies and from 2 human cases of paralytic rabies demonstrated only minor nucleotide differences. Deduced amino-acid patterns of the N protein were identical in both human and canine samples that came from the same geographic location, regardless of the clinical form. All differences in amino-acid patterns of the G protein were found outside the ectodomain, in either the signal peptide or the transmembrane and endodomains. None of the amino-acid differences of the P protein was within the interactive site with dynein. These findings support the concept that clinical manifestations of rabies are not explained solely by the associated rabies virus variant.