Adeno-associated viral vectors for the treatment of glycogen storage diseases
A carrier and virus technology, applied in the direction of virus/bacteriophage, virus, vector, etc., can solve the problem of not being able to completely correct liver G6Pase-α deficiency
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Embodiment 1
[0131] Example 1: Complete normalization of hepatic G6PC deficiency in glycogen storage disease type Ia using gene therapy
[0132] This example describes a comparison of the hepatic gene delivery efficiency and G6Pase-α expression of two G6Pase-α expressing AAV vectors driven by two different promoters in G6PC deficient mice. Results demonstrate that an AAV vector with a G6PC promoter / enhancer (AAV-GPE) is more efficient at directing durable in vivo hepatic transgene expression than an AAV vector with a chicken β-actin promoter / CMV enhancer (AAV-CBA) . In addition, G6PC-deficient mice treated with AAV-GPE exhibited normal levels of blood glucose, blood metabolites, liver glycogen, and liver fat.
[0133] Materials and methods
[0134] Construction of pUF11-GPE-G6PC and preparation of AAV vector
[0135] pUF11-mG6Pase-α-CBA (Ghosh et al., Gene Ther13:321-329, 2006) (wherein, mouse G6Pase-α is driven by CBA promoter / CMV enhancer (Xu et al., Hum Gene Ther 12:563-573, 2001)) ...
Embodiment 2
[0186] Example 2: Prevention of hepatocellular adenoma and correction of metabolic abnormalities in type IA glycogen storage disease using gene therapy
[0187] This example describes studies evaluating the efficacy of AAV-GPE vectors in long-term studies. G6pc - / - AAV-GPE vector-mediated gene therapy in mice was effective for at least 70-90 weeks in mice expressing greater than 3% of wild-type hepatic G6Pase-α. The results demonstrated that AAV-GPE-treated mice exhibited normal hepatic fat storage, normal blood metabolites and glucose tolerance profiles, reduced fasting blood insulin levels, and no signs of liver abnormalities.
[0188] Materials and methods
[0189] To G6pc - / - Mice infused with AAV-GPE
[0190] AAV-GPE vector (as described in Example 1, Yiu et al., Mol Ther 18:1076-1084, 2010) was infused into G6pc via the retro-orbital sinus - / - in mice (Lei et al., Nat Genet 13:203-209, 1996). Use an age-matched G6pc + / + / G6pc + / - and 6- to 10-week-old G6pc - / - M...
Embodiment 3
[0225] Example 3: The upstream enhancer element of the G6PC promoter is optimal for type Ia glycogen storage disease
[0226] G6PC expression is critical
[0227]The studies described in this example further evaluated the efficacy of AAV-GPE vectors. AAV-GPE is a single-stranded vector containing a G6PC promoter / enhancer of 2684bp compared to the double-stranded vector AAV-miGPE containing a minimal G6PC promoter / enhancer of 382bp. The results described in this example demonstrate that AAV-GPE vectors direct significantly higher levels of hepatic G6Pase-α expression in GSD-Ia mice compared to AAV-miGPE vectors, resulting in greater hepatic glycogen accumulation. and better fasting tolerance.
[0228] Materials and methods
[0229] Infusion of rAAV vectors into G6pc- / - mice
[0230] All G6pc- / - mice were kept alive by glucose therapy (Lei et al., Nat. Genet. 13:203-209, 1996). The rAAV vector was infused into 2-week-old G6pc- / - mice via the retro-orbital sinus. Use an age...
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