ArticleJournal of virology1996
The role of human adenovirus early region 3 proteins (gp19K, 10.4K, 14.5K, and 14.7K) in a murine pneumonia model.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed.
- Review
- Review
- Human Adenovirus Type 4 Comprises Two Major Phylogroups with Distinct Replicative Fitness and Virulence Phenotypes.Journal of virology · 2022Article
- Mechanisms of pathogenesis of emerging adenoviruses.F1000Research · 2017Review
- Unabated adenovirus replication following activation of the cGAS/STING-dependent antiviral response in human cells.Journal of virology · 2014Article
- Novel permissive murine immunocompetent orthotopic colon carcinoma model for comparison of the antitumoral and safety profiles of three Adv-TKs.Gene therapy · 2014Article
- No evidence of a death-like function for species B1 human adenovirus type 3 E3-9K during A549 cell line infection.BMC research notes · 2012Article
- Interference with intraepithelial TNF-α signaling inhibits CD8(+) T-cell-mediated lung injury in influenza infection.Viral immunology · 2010Article
- Open reading frame E3-10.9K of subspecies B1 human adenoviruses encodes a family of late orthologous proteins that vary in their predicted structural features and subcellular localization.Journal of virology · 2010Article
- Article
- Human adenovirus type 37 and the BALB/c mouse: progress toward a restricted adenovirus keratitis model (an American Ophthalmological Society thesis).Transactions of the American Ophthalmological Society · 2006Article
- Functional interactions of antiapoptotic proteins and tumor necrosis factor in the context of a replication-competent adenovirus.Gene therapy · 2005Article
- Linked tumor-selective virus replication and transgene expression from E3-containing oncolytic adenoviruses.Journal of virology · 2005Article
- Inhibition of chemokine expression by adenovirus early region three (E3) genes.Journal of virology · 2002Article
- Characterization of Ad5 E3-14.7K, an adenoviral inhibitor of apoptosis: structure, oligomeric state, and metal binding.Protein science : a publication of the Protein Society · 2002Article
- Review
- Inhibition of TRAIL-induced apoptosis and forced internalization of TRAIL receptor 1 by adenovirus proteins.Journal of virology · 2001Article
- Current research on respiratory viral infections: Third International Symposium.Antiviral research · 2001Review
- Clinical research results with dl1520 (Onyx-015), a replication-selective adenovirus for the treatment of cancer: what have we learned?Gene therapy · 2001Review
- Replication-selective oncolytic adenoviruses: virotherapy aimed at genetic targets in cancer.Oncogene · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Products of human adenovirus (Ad) early region 3 (E3) inhibit both specific (cytotoxic T lymphocytes [CTLs]) and innate (tumor necrosis factor alpha [TNF-alpha]) immune responses in vitro. The E3 gp19K protein prevents CTL recognition of Ad-infected fibroblasts by sequestering major histocompatibility complex class I proteins in the endoplasmic reticulum. E3 proteins 10.4K, 14.5K, and 14.7K function to protect infected cells from TNF-alpha cytolysis. To address the in vivo functions of these proteins, Ad mutants that lack the E3 genes encoding these proteins were inoculated intranasally into C57BL/10SnJ (H-2b) mice. Mutants that lack the gp19K gene failed to alter CTL generation or to affect Ad-induced pulmonary infiltrates. Since gamma interferon (IFN-gamma) is capable of overcoming gp19K suppression of CTL lysis in vitro, mice were depleted of IFN-gamma and inoculated with gp19K mutants. Even when IFN-gamma was depleted, gp19K was incapable of altering pulmonary lesions. These resuls are not in accord with the function of gp19K in vitro and suggest that gp19K does not affect immune recognition in vivo during an acute virus infection, yet they do not exclude the possibility that gp19K blocks immune recognition of Ad during a persistent infection. In contrast, when mice were inoculated with Ad mutants that lack the TNF resistance genes (14.7K and either 10.4K or 14.5K), there was a marked increase in alveolar infiltration and no change in the amounts of perivascular/peribronchiolar infiltration compared with wild-type-Ad-induced pathology. These findings demonstrate the importance of TNF susceptibility and TNF by-products for recruiting inflammatory cells into the lungs during Ad infections.
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Registered trials
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