Linked Life Data

16005263

Source:http://linkedlifedata.com/resource/pubmed/id/16005263

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pubmed-article:16005263pubmed:abstractTextGlycogen storage disease type II (GSD-II; Pompe disease) is caused by a deficiency of acid alpha-glucosidase (GAA; acid maltase) and manifests as muscle weakness, hypertrophic cardiomyopathy, and respiratory failure. Adeno-associated virus vectors containing either a liver-specific promoter (LSP) (AAV-LSPhGAApA) or a hybrid CB promoter (AAV-CBhGAApA) to drive human GAA expression were pseudotyped as AAV8 and administered to immunocompetent GAA-knockout mice. Secreted hGAA was detectable in plasma between 1 day and 12 weeks postadministration with AAV-LSPhGAApA and only from 1 to 8 days postadministration for AAV-CBGAApA. No anti-GAA antibodies were detected in response to AAV-LSPhGAApA (<1:200), whereas AAV-CBhGAApA provoked an escalating antibody response starting 2 weeks postadministration. The LSP drove approximately 60-fold higher GAA expression than the CB promoter in the liver by 12 weeks following vector administration. Furthermore, the detected cellular immunity was provoked by AAV-CBhGAApA, as detected by ELISpot and CD4+/CD8+ lymphocyte immunodetection. GAA activity was increased to higher than normal and glycogen content was reduced to essentially normal levels in the heart and skeletal muscle following administration of AAV-LSPhGAApA. Therefore, liver-restricted GAA expression with an AAV vector evaded immunity and enhanced efficacy in GSD-II mice.lld:pubmed
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pubmed-article:16005263pubmed:articleTitleEvasion of immune responses to introduced human acid alpha-glucosidase by liver-restricted expression in glycogen storage disease type II.lld:pubmed
pubmed-article:16005263pubmed:affiliationDivision of Medical Genetics, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA.lld:pubmed
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pubmed-article:16005263pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
pubmed-article:16005263pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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