ArticleJournal of virology1999
The replicative capacities of large E1B-null group A and group C adenoviruses are independent of host cell p53 status.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 124 citations in OpenAlex.
- Intravenous infusion of a replication-selective adenovirus (ONYX-015) in cancer patients: safety, feasibility and biological activity.Gene therapy · 2001Trial
- Immunological Impact of Oncolytic Adenoviruses On Cancer Therapy: Clinical Insights.European journal of immunology · 2025Review
- Advances in oncolytic herpes simplex virus and adenovirus therapy for recurrent glioma.Frontiers in immunology · 2023Review
- The human adenovirus type 5 E1B 55kDa protein interacts with RNA promoting timely DNA replication and viral late mRNA metabolism.PloS one · 2019Article
- Comparison of protein expression during wild-type, and E1B-55k-deletion, adenovirus infection using quantitative time-course proteomics.The Journal of general virology · 2017Article
- Reduced infectivity of adenovirus type 5 particles and degradation of entering viral genomes associated with incomplete processing of the preterminal protein.Journal of virology · 2012Article
- Timely synthesis of the adenovirus type 5 E1B 55-kilodalton protein is required for efficient genome replication in normal human cells.Journal of virology · 2012Article
- Chapter One---Cancer terminator viruses and approaches for enhancing therapeutic outcomes.Advances in cancer research · 2012Review
- The human adenovirus type 5 E1B 55 kDa protein obstructs inhibition of viral replication by type I interferon in normal human cells.PLoS pathogens · 2012Article
- Infection with E1B-mutant adenovirus stabilizes p53 but blocks p53 acetylation and activity through E1A.Oncogene · 2011Article
- Adenovirus E1B 55-kilodalton protein: multiple roles in viral infection and cell transformation.Journal of virology · 2009Review
- Phase I clinical trial of locoregional administration of the oncolytic adenovirus ONYX-015 in combination with mitomycin-C, doxorubicin, and cisplatin chemotherapy in patients with advanced sarcomas.Methods in molecular biology (Clifton, N.J.) · 2009Article
- A role for E1B-AP5 in ATR signaling pathways during adenovirus infection.Journal of virology · 2008Article
- Comparison of herpes simplex virus- and conditionally replicative adenovirus-based vectors for glioblastoma treatment.Cancer gene therapy · 2007Article
- Adenovirus ubiquitin-protein ligase stimulates viral late mRNA nuclear export.Journal of virology · 2007Article
- Genetic identification of adenovirus type 5 genes that influence viral spread.Journal of virology · 2006Article
- Adenovirus E1B 55-kilodalton protein is required for both regulation of mRNA export and efficient entry into the late phase of infection in normal human fibroblasts.Journal of virology · 2006Article
- Viruses - seeking and destroying the tumor program.Oncogene · 2005Review
- Clinical trials: the sensitizing side of ONYX-015.Gene therapy · 2005Article
- Oncolytic viral therapies.Cancer gene therapy · 2004Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent reports suggest that an early region 1B (E1B) 55, 000-molecular-weight polypeptide (55K)-null adenovirus type 5 (Ad5) mutant (dl1520) can replicate to the same extent as wild-type (wt) Ad5 in cells either deficient or mutated in p53, implicating p53 in limiting viral replication in vivo. In contrast, we show here that the replicative capacity of Ad5 dl1520 is wholly independent of host cell p53 status, as is the replicative capacity of comparable Ad12 E1B 54K-null adenoviruses (Ad12 dl620 and Ad12 hr703). Furthermore, we show that there is no requirement for complex formation between p53 and Ad5 E1B 55K or Ad12 E1B 54K for a productive infection, such that wt Ad5 and wt Ad12 will both replicate in cells which are null for p53. In addition, we find that these Ad5 and Ad12 mutant viruses induce S phase irrespective of the p53 status of the cell and that, therefore, S-phase induction does not correlate with the replicative capacity of the virus. Interestingly, the replicative capacities of the large E1B-null adenoviruses correlated positively with the ability to express E1B 19K and were related to the ability to repress premature adenovirus-induced apoptosis. Infection of primary human cells indicated that Ad5 dl1520, wt Ad5, and wt Ad12 replicated better in cycling normal human skin fibroblasts (HSFs) than in quiescent HSFs. Thus, the cell cycle status of the host cell, upon infection, also influences viral yield.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.