What is Poliovirus, Which is detected near New York City
Following the discovery of the poliovirus in yet another county’s wastewater in the vicinity of New York City, New York Governor Kathy Hochul announced Friday that the state was speeding up its polio-fighting efforts.
After the first case of polio in the United States in nearly a decade was discovered in July in Rockland County, which is north of the city, health officials started looking for the virus in sewage water. The most recent discovery involves a wastewater sample that was taken in Nassau County, on Long Island, to the east of the city, last month.
State health officials said the sample, which is genetically connected to the Rockland polio case, gives additional proof of the disease’s spreading throughout the population.
In the past, the poliovirus had been found in wastewater in the three counties to the north of New York City: Rockland, Orange, and Sullivan.
In accordance with Hochul’s declaration of a state of disaster, polio vaccinations may now be given by EMS personnel, midwives, and pharmacists, and doctors may now write standing polio vaccination orders. To concentrate vaccination efforts where they are most needed, data on immunizations will be used.
Dr. Mary T. Bassett, the state’s health commissioner, said in a prepared statement, “On polio, we just cannot play the dice.” “The risk of paralytic disease is real if you or your child are not up to date on immunizations. I urge New Yorkers to not tolerate any risk at all.”
All unvaccinated New York citizens, including babies under two months old, pregnant women, and those who haven’t finished their vaccine series, according to health officials, should get inoculated right away.
They recommended boosters for a few specific groups of people, including as medical professionals who work in impacted areas and treat patients who may have polio.
Although the rate of polio vaccination across the state is 79%, it was lower in the counties of Rockland, Orange, and Sullivan.
According to officials, it’s likely that hundreds of residents in the state have contracted polio but are unaware of it. Most polio sufferers don’t show any symptoms, yet they can still spread the disease for a few days or weeks.
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One anonymous young adult who was unvaccinated was the subject of the lone verified case in New York.
The poliovirus, also known as poliomyelitis or enterovirus C, is a kind of the Picornaviridae family’s species Enterovirus C. It is the cause of poliomyelitis. There are three different forms of the poliovirus: 1, 2, and 3.
A protein capsid and an RNA genome make up the poliovirus. The genome is a 7500 nucleotide single-stranded positive-sense RNA (+ssRNA) genome. The viral particle has icosahedral symmetry and measures around 30 nm in diameter.
The poliovirus is commonly recognised as the simplest important virus due to its tiny genome and basic structure, which consists solely of RNA and an icosahedral protein coat that encases it.
Karl Landsteiner and Erwin Popper discovered the poliovirus for the first time in 1909.
A team at Birkbeck College led by Rosalind Franklin initially used X-ray diffraction to determine the virus’s structure, revealing that it has icosahedral symmetry.
Two distinct research groups—Vincent Racaniello and David Baltimore at MIT and Naomi Kitamura and Eckard Wimmer at Stony Brook University—published the poliovirus genome in 1981.
James Hogle used X-ray crystallography to identify the three-dimensional structure of the poliovirus at Scripps Research Institute in 1985.
One of the most thoroughly studied viruses, the poliovirus is now used as a model system to study the biology of RNA viruses.
An immunoglobulin-like receptor on the cell surface called CD155, sometimes referred to as the poliovirus receptor or PVR, is how the poliovirus infects human cells.
The irreversible conformational shift of the viral particle required for viral entrance is made possible by interaction between the poliovirus and CD155.
The viral nucleic acid was assumed to enter the host cell cytoplasm after adhering to the membrane in one of two ways: either by creating a breach in the plasma membrane through which the RNA is subsequently “injected” into the cell, or by being taken up through receptor-mediated endocytosis.
The latter theory is supported by recent experimental data, which indicates that the poliovirus attaches to CD155 and is taken up by endocytosis. The viral RNA is released right away when the particle is internalised.
A positive-stranded RNA virus is the poliovirus. As a result, the host cell can employ the viral particle’s genome as messenger RNA and begin translating it right away. Upon infection, the virus takes over the cell’s translational apparatus, inhibiting cellular protein synthesis in favour of the generation of virus-specific proteins.
The 5′ end of the poliovirus RNA is almost 700 nucleotides long and highly organised, unlike the mRNAs of the host cell. An internal ribosome entrance site is the term for this section of the viral genome (IRES). Three or four domains and numerous secondary components make up this region.
A self-folding RNA element called domain 3 has a number of stable stem loops connected by two four-way junctions that include conserved structural motifs.
IRES is made up of numerous domains, and each of these domains contains numerous loops that use ribosomes as a means of modified translation in the absence of a 5′ end cap. The GNRA tetraloop is the name of domain 3’s interaction loop.
Adenosine residues A180 and A181 in the GUAA tetraloop engage with the receptor base pairs C230/G242 and G231/C241, respectively, to create hydrogen bonds through non-canonical base pairing interactions.
Genetic changes in this area stop the viral protein from being produced. Poliovirus RNA contained the first IRES to be detected.
One lengthy polypeptide is produced after poliovirus mRNA translation. Internal proteases then autocleave this polypeptide into roughly 10 distinct viral proteins. Not all cleavages take place as effectively as others.
As a result, different proteins are created in different quantities by the polypeptide cleavage. For instance, less 3Dpol and more VP1-4, which are capsid proteins, are produced. These specific viral proteins include:
The poliovirus type 1 genomic structure
The purpose of the RNA dependent RNA polymerase 3Dpol is to produce many copies of the viral RNA genome.
The proteases 2Apro and 3Cpro/3CDpro cleave the viral polypeptide.
VPg (3B), a tiny protein required for the production of viral positive and negative strand RNA, binds viral RNA.
Proteins 2BC, 2B, 2C (an ATPase), 3AB, 3A, and 3B make up the complex of proteins required for viral replication.
VP0, which is further broken down into the viral capsid proteins VP1 and VP3, VP2 and VP4, and VP3,