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vol.11 número2REPLICACIÓN DEL HERPESVIRUS EQUINO Y SU ASOCIACIÓN CON LA PATOGÉNESIS MOLECULARRIBONUCLEASAS: [subtitle]SU POTENCIAL TERAPÉUTICO EN INFECCIONES VIRALES índice de autoresíndice de materiabúsqueda de artículos
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Acta Biológica Colombiana

versión impresa ISSN 0120-548X

Resumen

PRADAARISMENDY, JEANETTE  y  CASTELLANOS, JAIME E. Susceptibility/Resistance Genes to Flavivirus, Implications on Disease Severity. Acta biol.Colomb. [online]. 2006, vol.11, n.2, pp.21-30. ISSN 0120-548X.

Flavivirus caused infections are among the diseases with the highest incidence in the world. Most of these infections have a wide severity clinical profile, from unspecific fever to lethal hemorrhages and encephalitis. The reason of the clinical variability remains unclear, but it appears to be associated to host genetic features. Susceptible or resistant mouse strains to Flavivirus infection have been identified and the gene responsible for this has been mapped by positional cloning as the West Nile Virus susceptibility mouse gene in chromosome 5, that codifies for Oligoadenylate Synthetase, isoform 1b (OAS1b). OAS produces adenine oligomers that activate endoribonuclease RNAseL to degrade viral RNA. Resistant mice strains produce significantly less virus than susceptible ones. In humans, it has recently been reported a single nucleotide polymorphism associated with susceptibility to West Nile Virus infection in the OASL gene. However, the biochemical or molecular mechanisms that explained this susceptibility are not clear. Further knowledge related with these processes is important for understanding flaviviral pathogenesis and for the design of therapeutic alternatives.

Palabras clave : Dengue; Oligoadenylate Synthetase; Flavivirus; mouse; innate susceptibility.

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