ArticleDrug delivery and translational research2022
A recombinant adenoviral vector with a specific tropism to CD4-positive cells: a new tool for HIV-1 inhibition.
Article in Drug delivery and translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Tat-dependent conditionally replicating adenoviruses expressing diphtheria toxin A for specifically killing HIV-1-infected cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Nanoparticles exhibiting virus-mimic surface topology for enhanced oral delivery.Nature communications · 2023Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene therapy can be an option to overcome the side effects of chemotherapy and prevent the development of drug-resistant HIV viruses in HIV-infected patients. The need to develop a safe and efficient vector for gene transfer is always necessary and an appropriate option might be adenovirus (Ad). The use of Ad vectors in gene delivery applications is limited due to the semi-specific tropism. A strategy to overcome this tropism limitation may be the modification of the fiber protein domain involved in the viral binding to cells. Therefore, we designed an Ad5 vector with a specific tropism to CD4 + cells containing an expression system limited to HIV-infected cells. We replaced the knob region of Ad5 fiber protein with the extracellular region of the HIV-1 envelope. We also used a specific Tat-inducible promoter to express two anti-HIV-1 shRNAs. Tropism of recombinant Ad5 was assayed by a comparison of the shRNA expression level in CEM and PBMC cells (as CD4 + cells) and HEK293 cells (as CD4 cells). HIV-1 inhibition was assayed by the determination of p24 antigen in the HIV-infected CEM cells transduced with the recombinant Ad5 vector. Our results showed that the shRNA expression was significantly higher in CEM and PBMC cells than HEK293 cells when transduced with recombinant Ad5 vector. This new Ad5 vector also inhibited HIV-1 proliferation in a Tat-inducible manner. Our new recombinant Ad5 vector has a specific tropism to CD4-positive cells that can effectively suppress the HIV-1 replication.
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