ArticleVirology journal2009
Genetic reconstitution of the human adenovirus type 2 temperature-sensitive 1 mutant defective in endosomal escape.
Article in Virology journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Rab9 depletion enhances human adenovirus type 26 transduction efficiency through increased internalization and reduced late endosomal/lysosomal retention.PLoS pathogens · 2026Article
- Transcriptional transactivation turns human iPSC-derived macrophages into an adenovirus-producing cell state.Journal of virology · 2026Article
- Adenovirus maturation establishes the transcription competent packaging of its genome.EMBO reports · 2025Article
- Article
- Mysteries of adenovirus packaging.Journal of virology · 2025Review
- A recombinant virus-like particle vaccine against adenovirus-7 induces a potent humoral response.NPJ vaccines · 2023Article
- Adenovirus core protein V reinforces the capsid and enhances genome release from disrupted particles.Science advances · 2023Article
- The Revolving Door of Adenovirus Cell Entry: Not All Pathways Are Equal.Pharmaceutics · 2021Review
- IgG-Complexed Adenoviruses Induce Human Plasmacytoid Dendritic Cell Activation and Apoptosis.Viruses · 2021Article
- Virus Infection Variability by Single-Cell Profiling.Viruses · 2021Review
- Microscopy deep learning predicts virus infections and reveals mechanics of lytic-infected cells.iScience · 2021Article
- The FDA-Approved Drug Nelfinavir Inhibits Lytic Cell-Free but Not Cell-Associated Nonlytic Transmission of Human Adenovirus.Antimicrobial agents and chemotherapy · 2020Article
- Dynamic competition for hexon binding between core protein VII and lytic protein VI promotes adenovirus maturation and entry.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Humoral immune response to adenovirus induce tolerogenic bystander dendritic cells that promote generation of regulatory T cells.PLoS pathogens · 2018Article
- Article
- The adenovirus major core protein VII is dispensable for virion assembly but is essential for lytic infection.PLoS pathogens · 2017Article
- Insights into Adenovirus Uncoating from Interactions with Integrins and Mediators of Host Immunity.Viruses · 2016Review
- The amphipathic helix of adenovirus capsid protein VI contributes to penton release and postentry sorting.Journal of virology · 2015Article
- Review
- Coat as a dagger: the use of capsid proteins to perforate membranes during non-enveloped DNA viruses trafficking.Viruses · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human adenoviruses infect the upper and lower respiratory tracts, the urinary and digestive tracts, lymphoid systems and heart, and give rise to epidemic conjunctivitis. More than 51 human serotypes have been identified to-date, and classified into 6 species A-F. The species C adenoviruses Ad2 and Ad5 (Ad2/5) cause upper and lower respiratory disease, but how viral structure relates to the selection of particular infectious uptake pathways is not known. An adenovirus mutant, Ad2-ts1 had been isolated upon chemical mutagenesis in the past, and shown to have unprocessed capsid proteins. Ad2-ts1 fails to package the viral protease L3/p23, and Ad2-ts1 virions do not efficiently escape from endosomes. It had been suggested that the C22187T point mutation leading to the substitution of the conserved proline 137 to leucine (P137L) in the L3/p23 protease was at least in part responsible for this phenotype. To clarify if the C22187T mutation is necessary and sufficient for the Ad2-ts1 phenotype, we sequenced the genes encoding the structural proteins of Ad2-ts1, and confirmed that the Ad2-ts1 DNA carries the point mutation C22187T. Introduction of C22187T to the wild-type Ad2 genome in a bacterial artificial chromosome (Ad2-BAC) gave Ad2-BAC46 virions with the full Ad2-ts1 phenotype. Reversion of Ad2-BAC46 gave wild-type Ad2 particles indicating that P137L is necessary and sufficient for the Ad2-ts1 phenotype. The kinetics of Ad2-ts1 uptake into cells were comparable to Ad2 suggesting similar endocytic uptake mechanisms. Surprisingly, infectious Ad2 or Ad5 but not Ad2-ts1 uptake required CALM (clathrin assembly lymphoid myeloid protein), which controls clathrin-mediated endocytosis and membrane transport between endosomes and the trans-Golgi-network. The data show that no other mutations than P137L in the viral protease are necessary to give rise to particles that are defective in capsid processing and endosomal escape. This provides a basis for genetic analyses of distinct host requirements for Ad endocytosis and escape from endosomes.
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Registered trials
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