ArticleScientific reports2016
Influence of cell physiological state on gene delivery to T lymphocytes by chimeric adenovirus Ad5F35.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- The dynamics of chemoattractant receptors redistribution in the electrotaxis of 3T3 fibroblasts.Cell communication and signaling : CCS · 2025Article
- Engineered cell therapies for autoimmune diseases: evaluating CAR-T and CAR-M progress and prospects.Frontiers in immunology · 2025Review
- Designing molecules: directing stem cell differentiation.Frontiers in bioengineering and biotechnology · 2024Review
- Efficient Editing of an Adenoviral Vector Genome with CRISPR/Cas9.Indian journal of microbiology · 2021Article
- Article
- Gene Therapy Leaves a Vicious Cycle.Frontiers in oncology · 2019Review
- Plasma from some cancer patients inhibits adenoviral Ad5f35 vector transduction of dendritic cells.Cytotherapy · 2018Article
- Blood Coagulation Factor X Exerts Differential Effects on Adenovirus Entry into Human Lymphocytes.Viruses · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adoptive transfer of genetically-modified T cells is a promising approach for treatment of both human malignancies and viral infections. Due to its ability to efficiently infect lymphocytes, the chimeric adenovirus Ad5F35 is potentially useful as an immunotherapeutic for the genetic modification of T cells. In previous studies, it was found that the infection efficiency of Ad5F35 was significantly increased without enhanced expression of the viral receptor after T cell stimulation; however, little is known about the underlying mechanism. Nonetheless, cell physiology has long been thought to affect viral infection. Therefore, we aimed to uncover the physiologic changes responsible for the increased infection efficiency of Ad5F35 following T cell stimulation. Given the complexity of intracellular transport we analyzed viral binding, entry, and escape using a Jurkat T cell model and found that both cell membrane fluidity and endosomal escape of Ad5F35 were altered under different physiological states. This, in turn, resulted in differences in the amount of virus entering cells and reaching the cytoplasm. These results provide additional insight into the molecular mechanisms underlying Ad5F35 infection of T cells and consequently, will help further the clinical application of genetically-modified T cells for immunotherapy.
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