ArticleJournal of virology2007
Minor capsid proteins of simian virus 40 are dispensable for nucleocapsid assembly and cell entry but are required for nuclear entry of the viral genome.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 45 citations in OpenAlex.
- Discovery of novel druggable pockets on polyomavirus VP1 through crystallographic fragment-based screening to develop capsid assembly inhibitors.RSC chemical biology · 2022Article
- BK Polyomavirus Requires the Mismatch Repair Pathway for DNA Damage Response Activation.Journal of virology · 2022Article
- Revealing in real-time a multistep assembly mechanism for SV40 virus-like particles.Science advances · 2020Article
- Association Between Simian Virus 40 and Human Tumors.Frontiers in oncology · 2019Review
- Effect of dsDNA on the Assembly Pathway and Mechanical Strength of SV40 VP1 Virus-like Particles.Biophysical journal · 2018Article
- BK Polyomavirus: Clinical Aspects, Immune Regulation, and Emerging Therapies.Clinical microbiology reviews · 2017Review
- Nuclear Import of Hepatitis B Virus Capsids and Genome.Viruses · 2017Review
- Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity.Oncotarget · 2016Article
- Nuclear entry of DNA viruses.Frontiers in microbiology · 2015Review
- Coat as a dagger: the use of capsid proteins to perforate membranes during non-enveloped DNA viruses trafficking.Viruses · 2014Review
- Formation of covalently modified folding intermediates of simian virus 40 Vp1 in large T antigen-expressing cells.Journal of virology · 2013Article
- The Merkel cell polyomavirus minor capsid protein.PLoS pathogens · 2013Article
- BK polyomavirus: emerging pathogen.Microbes and infection · 2012Review
- Simian virus 40 transformation, malignant mesothelioma and brain tumors.Expert review of respiratory medicine · 2011Review
- Glycosaminoglycans and sialylated glycans sequentially facilitate Merkel cell polyomavirus infectious entry.PLoS pathogens · 2011Article
- A large and intact viral particle penetrates the endoplasmic reticulum membrane to reach the cytosol.PLoS pathogens · 2011Article
- Learning from the viral journey: how to enter cells and how to overcome intracellular barriers to reach the nucleus.The AAPS journal · 2009Review
- Article
- Simian virus 40 induces lamin A/C fluctuations and nuclear envelope deformation during cell entry.Nucleus (Austin, Tex.)Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We investigated the roles of simian virus 40 capsid proteins in the viral life cycle by analyzing point mutants in Vp1 and Vp2/3, as well as a deletion mutant lacking the Vp2/3 coding sequence. The Vp1 mutants (V243E and L245E) and the Vp2/3 mutants (F157E-I158E and P164R-G165E-G166R) were previously shown to be defective in Vp1-Vp2/3 interaction and to be noninfectious or poorly infectious, respectively. Here, we show that all these point mutants form stable particles following DNA transfection into cells. The Vp2/3-mutant particles contained very low levels of Vp2/3, whereas the Vp1 mutant particles contained no detectable Vp2/3. As expected, the deletion mutant also formed particles that were noninfectious. We further characterized the two Vp1 point mutants and the deletion mutant. All three mutant particles comprised Vp1 and histone-associated viral DNA, and all were able to enter cells. However, the mutant complexes failed to associate with host importins (owing to the loss of the Vp2/3 nuclear localization signal), and the mutant viral DNAs prematurely dissociated from the Vp1s, suggesting that the nucleocapsids did not enter the nucleus. Consistently, all three mutant particles failed to express large T antigen. Together, our results demonstrate unequivocally that Vp2/3 is dispensable for the formation of nucleocapsids. Further, the nucleocapsids' ability to enter cells implies that Vp1 contains the major determinants for cell attachment and entry. We propose that the major role of Vp2/3 in infectivity is to mediate the nuclear entry of viral DNA.
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Registered trials
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.