This item requires custom production and lead time is between 4-12 weeks. We can custom produce based on your specifications.
Purity
>85%
Format
Liquid
Buffer
50mMTris-HCl, 200mMNaCl, 2M Urea, pH8.0
Preservative
None
Storage
Store at 2-8 °C short term and -80°C long term. It is recommended to aliquot needed volumes and store at -80°C. Avoid repeated freeze/thaw cycles.
Introduction
Poliovirus, the causative agent of polio (also known as poliomyelitis), is a serotype of the species Enterovirus C, in the family of Picornaviridae. Poliovirus is composed of an RNA genome and a protein capsid. The genome is a single-stranded positive-sense RNA (+ssRNA) genome that is about 7500 nucleotides long. The viral particle is about 30 nm in diameter with icosahedral symmetry. Because of its short genome and its simple composition-only RNA and a nonenveloped icosahedral protein coat that encapsulates it, poliovirus is widely regarded as the simplest significant virus.
Antigen Description
Recombinant 6xHis tagged Poliovirus type 1 Capsid protein (strain Sabin) (UniProtKB No. M1VMR5) was expressed.
Keywords
Capsid protein;Poliovirus type 1;VP1
Citations
Publication ()
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Background
Poliovirus, the pathogen of polio, destroys motor neurons in the central nervous system, leading to paralysis and even death. Of these, wild-type poliovirus type 1 remains endemic in Afghanistan, Nigeria and Pakistan, while wild poliovirus type 2 has not been detected worldwide since 1999. Poliovirus, with its small size and simple structure, is a human enterovirus that has been extensively studied. It enters human cells by binding to the immunoglobulin-like receptor CD155 and by endocytosis, and is more readily translated upon entering the cell because of its positive-stranded RNA genome. Poliovirus hijacks cells by producing proteases that disrupt cap-binding proteins, and translation of viral mRNAs is not dependent on the cap structure, so host cell translators are completely dedicated to the production of viral proteins. Inhibition of the host translation system contributes to virus-specific protein synthesis, ultimately leading to the production of a single viral long-chain protein, which in turn is cleaved by internal proteases into 10 viral proteins.
Poliovirus is considered to be one of the most rapidly evolving viruses, with an estimated total nucleotide substitution rate of approximately 0.01 substitutions per site per year in the capsid coding region. The evolution of this virus, like that of normal positive-stranded RNA viruses, is based on polymerase error-induced point mutations and recombination, followed by selection of mutants due to limitations in transmission routes. Simultaneously with the increase in mutations, this in turn produces mutant enrichment.
The final strategic plan for the global polio eradication campaign is currently in its final stages, and vaccination policy reforms are being implemented to ensure that the eradication campaign is completed and sustained. Polio vaccines currently in use include oral polio vaccine (OPV) and inactivated polio vaccine (IPV). Among them, OPV is the preferred vaccine, which is relatively inexpensive, easy to administer, induces gastrointestinal mucosal immunity in the body, and contributes greatly to the control of the incidence and prevalence of poliomyelitis. However, the potential exists for OPV to cause vaccine-derived poliovirus to circulate and regain virulence. IPV induces effective humoral immunity, allowing vaccinated individuals to fight the disease, but does not elicit sufficient mucosal immunity and prevent the proliferation of wild viruses in the intestinal tract, and is less efficient than OPV for protection in a population.
Figure 1. Global clinical trials of poliovirus vaccines in infants, children and adults (Source: Connor RI, et al. 2022)
References
1. Connor RI, et al. Mucosal immunity to poliovirus. Mucosal Immunol. 2022 Jan;15(1):1-9.
2. Quarleri J. Poliomyelitis is a current challenge: long-term sequelae and circulating vaccine-derived poliovirus. Geroscience. 2023 Apr;45(2):707-717.
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References
Tungsten carbide nanoparticles show a broad spectrum virucidal activity against enveloped and nonenveloped model viruses using a guideline-standardized in vitro test
Five tungsten carbide nanoparticle preparations (denoted WC1-WC5) were investigated for broad spectrum virucidal activity against four recommended model viruses. These are modified vaccinia virus Ankara (MVA), human adenovirus type 5 (HAdV-5), poliovirus type 1 (PV-1) and murine norovirus (MNV). All virucidal tests were performed two to five times using the quantitative suspension test, which is a highly standardized test method to evaluate the virucidal efficacy of disinfectants in accordance with the European norm EN 14476+A1 and the German DVV/RKI guidelines. Quantitative detection of viruses was conducted by endpoint titration and quantitative real-time PCR. Results showed that three of the five tested compounds (WC1-WC3) were able to reduce the infectivity of all model viruses by at least four log(10) of tissue culture infective dose 50% per ml after 15 min, whereas the other two compounds exhibited only limited efficacy (WC4) or showed cytotoxicity (WC5). Virucidal activity of nanoparticles increased with incubation time and a dose-effect curve showed dependence of virucidal activity with particle concentration. Whereas WC1-WC4 showed little cytotoxicity, WC5 which was doped with copper exhibited a significant cytotoxic effect. These findings propose tungsten carbide nanoparticles to be very promising in terms of new disinfection techniques. Significance and Impact of the Study The present study investigates the virucidal activity of tungsten carbide nanoparticles using the quantitative suspension test in accordance with the European norm EN 14476+A1 and the German DVV/RKI guidelines. Due to highly standardized assay conditions, results of this test are considered very reliable for evaluation of the virucidal activity of disinfectants. Broad-spectrum activity and high efficacy of three different tungsten carbide nanoparticles preparations is concluded.
Enterovirus particles expel capsid pentamers to enable genome release
Viruses from the genus Enterovirus are important human pathogens. Receptor binding or exposure to acidic pH in endosomes converts enterovirus particles to an activated state that is required for genome release. However, the mechanism of enterovirus uncoating is not well understood. Here, we use cryo-electron microscopy to visualize virions of human echovirus 18 in the process of genome release. We discover that the exit of the RNA from the particle of echovirus 18 results in a loss of one, two, or three adjacent capsid-protein pentamers. The opening in the capsid, which is more than 120 A in diameter, enables the release of the genome without the need to unwind its putative double-stranded RNA segments. We also detect capsids lacking pentamers during genome release from echovirus 30. Thus, our findings uncover a mechanism of enterovirus genome release that could become target for antiviral drugs.