Directed-evolution AAV capsid variants improve glioblastoma cell binding, tumor penetration, and gene transduction in glioma.
Targeted mutations in the AAV capsid 561-588 region improve tissue tropism and payload packaging for more efficient gene delivery.
Non-identical capsid half-dimers enable controlled asymmetric virus-like particle assembly, cargo loading, and addressable holey capsids.
HDAC inhibitor cell culture boosts rAAV yield two-fold or more, cutting GMP manufacturing cost and improving scale-up.
Engineered AAV capsid substitutions improve skeletal and cardiac muscle transduction while reducing brain and liver uptake and immune risk.
Specific VP1 capsid mutations improve AAV delivery to retinal pigment epithelium while preserving capsid integrity for intravitreal or subretinal use.
Targeted VP1 mutations in AAV capsids shift tropism and improve payload packaging for more precise and efficient gene delivery.
Deleting ICP6 and IR regions creates a replication-competent HSV-1 vector that accepts larger therapeutic genes and selectively kills cancer cells.
Synthetic anellovectors and anelloVLPs deliver therapeutic agents while reducing immune response and minimizing genomic integration.
LMP1-expressing B cells boost antigen presentation and prime broad T cell responses, helping overcome tumor antigen loss and weak checkpoint therapy.
Combining rep-cap and adenovirus helper genes into one plasmid simplifies transfection and boosts rAAV yield while cutting production time and cost.
By inactivating the HERV-K envelope ISD in adenoviral VLP vaccines, this case shows broader CD4/CD8 activation and tumor control.
High-affinity spike-binding antibodies neutralize virus infectivity and extend protection to newly identified coronaviruses.
Separate inducible Rep, Cap, and helper modules let packaging cells tune AAV titer, full capsid ratio, and cell health during production.
A dual-host plasmid strategy uses E. coli and B. subtilis amplification to improve virus-derived construct yield and vector genome copy number.
Specific AAV capsid residue changes modulate AAVR binding to reduce liver off-target transduction while preserving delivery to target tissues.
Peptide inserts in AAV capsid variable regions improve muscle tropism and specificity while reducing liver targeting in gene therapy.
Clinical HSV isolates are selected and engineered with fusogenic and immune-stimulatory genes to kill tumors faster and boost antitumor immunity.
Transient p53 inhibition boosts HDR in gene-edited hematopoietic stem cells, improving survival, engraftment, and editing efficiency.
Surface-exposed peptide inserts in rAAV capsids improve targeting to muscle, CNS, and retina while reducing liver transduction and dosing.
CMV Triplex vaccination expands dual-specific CAR T cells in vivo to improve persistence, engraftment, and anti-tumor activity after HCT.
Knocking out C1s protease in CHO cells prevents gp120 cleavage, raising yields of full-length HIV envelope proteins for vaccine production.
Modified VP1, VP2, and VP3 capsids limit deamidation during storage, helping AAV vectors retain purity, stability, and transduction efficiency.
Targeted capsid mutations shift AAV9 delivery toward cardiac cells while lowering liver transduction, dose burden, and inflammation.
Selective CRBN-binding compounds preserve target protein degradation while avoiding ASS1 recruitment, ubiquitination, and side effects.
Capsid-only anellovectors deliver therapeutic genetic cargo to eukaryotic cells while reducing immune response and minimizing genomic integration.
Combining adenoviral, HSV, and HBoV helper functions in one plasmid boosts infectious rAAV yield across serotypes and cell lines.
Differential codon bias in separate Rep52 and Rep78 sequences limits recombination in baculoviral insect-cell AAV production and improves yield stability.
Cell-type-specific promoters enable RNA-driven AAV capsid screening for targeted CNS transduction without transgenic animals.