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There was no evidence of viral vector infection of extraskeletal tissues, suggesting that this in vivo gene therapy for fracture repair is safe.
The insect cells that serve as hosts for baculovirus vector infection are capable of transferring oligosaccharide side chains (glycans) to the same sites in recombinant proteins as those that are used for native protein N‐glycosylation in mammalian cells.
An immunization scheme was designed for the sequential immunization of animals by direct vector injection followed by protein booster immunization using influenza HA produced in vitro from MVA vector infection of cells in culture.
Overexpression of cathepsin B attenuated the CD4-independent vector infection in 293T cells.
The TLR4 signal activation also attenuated the CD4-independent vector infection by enhancing cathepsin B expression.
These results show that cathepsin B inhibits the CD4-independent HIV-1 vector infection.
Hybridoma cells between HeLa and 293T cells were as susceptible to the mNDK vector infection as 293T cells, indicating that HeLa cells lack a cellular factor(s) required for the CD4-independent mNDK vector infection.
To address whether cystatin C enhances the CD4-independent HIV-1 vector infection by inhibiting cathepsin protease activity, the effects of synthetic cathepsin protease inhibitors on CD4-independent vector infection were analyzed.
Dynasore treatment more efficiently attenuated the CD4-independent mNDK vector infection than the CD4-dependent mNDK (Fig. 10A) or HXB2 (data not shown) vector infection in all examined cells (P<0.05).
To confirm that cathepsin B inhibits the CD4-independent vector infection, the effects of cathepsin B overexpression on the CD4-independent vector infection were analyzed in 293T cells, in which cathepsin B is expressed at a low level.
Cathepsin B activity was inversely correlated with cellular susceptibility to the CD4-independent HIV-1 vector infection.
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