ArticleVirology journal2011
Infection by agnoprotein-negative mutants of polyomavirus JC and SV40 results in the release of virions that are mostly deficient in DNA content.
Article in Virology journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Target-specific peptides for BK virus agnoprotein identified through phage display screening: advancing antiviral therapeutics.Scientific reports · 2025Article
- Recent advances in discovery and functional analysis of the small proteins and microRNA expressed by polyomaviruses.Virology · 2025Review
- Article
- Human neurotropic polyomavirus, JC virus, agnoprotein targets mitochondrion and modulates its functions.Virology · 2021Article
- Evidence of the Mechanism by Which Polyomaviruses Exploit the Extracellular Vesicle Delivery System during Infection.Viruses · 2020Review
- Expression of novel proteins by polyomaviruses and recent advances in the structural and functional features of agnoprotein of JC virus, BK virus, and simian virus 40.Journal of cellular physiology · 2019Review
- Neuroimmune Regulation of JC Virus by Intracellular and Extracellular Agnoprotein.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Article
- Discovery and characterization of novel trans-spliced products of human polyoma JC virus late transcripts from PML patients.Journal of cellular physiology · 2018Article
- Agnoprotein Is an Essential Egress Factor during BK Polyomavirus Infection.International journal of molecular sciences · 2018Article
- Structure-based release analysis of the JC virus agnoprotein regions: A role for the hydrophilic surface of the major alpha helix domain in release.Journal of cellular physiology · 2018Article
- Article
- Role of BK human polyomavirus in cancer.Infectious agents and cancer · 2018Review
- Nuclear Magnetic Resonance Structure of the Human Polyoma JC Virus Agnoprotein.Journal of cellular biochemistry · 2017Article
- Alcohol-Mediated Missplicing of Mcl-1 Pre-mRNA is Involved in Neurotoxicity.Alcoholism, clinical and experimental research · 2017Article
- Emerging From the Unknown: Structural and Functional Features of Agnoprotein of Polyomaviruses.Journal of cellular physiology · 2016Review
- Downregulation of the stress-induced ligand ULBP1 following SV40 infection confers viral evasion from NK cell cytotoxicity.Oncotarget · 2016Article
- Targeting the Channel Activity of Viroporins.Advances in protein chemistry and structural biology · 2016Review
- JC virus nucleotides 376-396 are critical for VP1 capsid protein expression.Journal of neurovirology · 2015Article
- Review
- Agnoprotein of polyomavirus BK interacts with proliferating cell nuclear antigen and inhibits DNA replication.Virology journal · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHuman polyomavirus JC (JCV) is the etiologic agent of a brain disease, known as progressive multifocal leukoencephalopathy (PML). The JCV genome encodes a small multifunctional phospho-protein, agnoprotein, from the late coding region of the virus, whose regulatory functions in viral replication cycle remain elusive. In this work, the functional role of JCV and SV40 agnoproteins in virion release was investigated using a point mutant (Pt) of each virus, where the ATG codon of agnoprotein was mutated to abrogate its expression.
resultsAnalysis of both viral protein expression and replication using Pt mutant of each virus revealed that both processes were substantially down-regulated in the absence of agnoprotein compared to wild-type (WT) virus. Complementation studies in cells, which are constitutively expressing JCV agnoprotein and transfected with the JCV Pt mutant genome, showed an elevation in the level of viral DNA replication near to that observed for WT. Constitutive expression of large T antigen was found to be not sufficient to compensate the loss of agnoprotein for efficient replication of neither JCV nor SV40 in vivo. Examination of the viral release process for both JCV and SV40 Pt mutants showed that viral particles are efficiently released from the infected cells in the absence of agnoprotein but were found to be mostly deficient in viral DNA content.
conclusionsThe results of this study provide evidence that agnoprotein plays an important role in the polyomavirus JC and SV40 life cycle. Infection by agnoprotein-negative mutants of both viruses results in the release of virions that are mostly deficient in DNA content.
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