Poliovirus

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Poliovirus
Polio.jpg
TEM micrograph of poliovirus virions. Scale bar (white): 50 nm
Polio-3-chains.png
A type 3 poliovirus capsid, protein side chains coloured
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Pisuviricota
Class: Pisoniviricetes
Order: Picornavirales
Family: Picornaviridae
Genus: Enterovirus
Species:
Enterovirus C
Virus:
Poliovirus
Serotypes

Poliovirus, the causative agent of polio (also known as poliomyelitis), is a serotype of the species Enterovirus C , in the family of Picornaviridae . [1] There are three poliovirus serotypes, numbered 1, 2, and 3.

Contents

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. [2] The viral particle is about 30 nm in diameter with icosahedral symmetry. Because of its short genome and its simple composition—only a strand of RNA and a nonenveloped icosahedral protein coat encapsulating it—poliovirus is widely regarded as the simplest significant virus. [3]

Poliovirus is one of the most well-characterized viruses, and has become a useful model system for understanding the biology of RNA viruses.

Replication cycle

The replication cycle of poliovirus is initiated by binding to the cell surface receptor CD155 (1). The virion forms a pore in the cell membrane through which viral RNA is released into the cytoplasm (2). Translation of the viral RNA occurs by an IRES-mediated mechanism (3). The polyprotein is cleaved, yielding mature viral proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, producing double-stranded replicative form (RF) RNA (5). Many positive strand RNA copies are produced from the single negative strand (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation of more viral proteins (7) or can be enclosed in a capsid (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9). Poliovirus life cycle.png
The replication cycle of poliovirus is initiated by binding to the cell surface receptor CD155 (1). The virion forms a pore in the cell membrane through which viral RNA is released into the cytoplasm (2). Translation of the viral RNA occurs by an IRES-mediated mechanism (3). The polyprotein is cleaved, yielding mature viral proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, producing double-stranded replicative form (RF) RNA (5). Many positive strand RNA copies are produced from the single negative strand (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation of more viral proteins (7) or can be enclosed in a capsid (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).

Poliovirus infects human cells by binding to an immunoglobulin-like receptor, CD155 (also known as the poliovirus receptor or PVR) [5] [6] on the cell surface. [7] Interaction of poliovirus and CD155 facilitates an irreversible conformational change of the viral particle necessary for viral entry. [8] [9] Following attachment to the host cell membrane, entry of the viral nucleic acid was thought to occur one of two ways: via the formation of a pore in the plasma membrane through which the RNA is then "injected" into the host cell cytoplasm, or via virus uptake by receptor-mediated endocytosis. [10] Recent experimental evidence supports the latter hypothesis and suggests that poliovirus binds to CD155 and is taken up by endocytosis. Immediately after internalization of the particle, the viral RNA is released. [11]

Poliovirus is a positive-stranded RNA virus. Thus, the genome enclosed within the viral particle can be used as messenger RNA and immediately translated by the host cell. On entry, the virus hijacks the cell's translation machinery, causing inhibition of cellular protein synthesis in favor of virus-specific protein production. [12] Unlike the host cell's mRNAs, the 5' end of poliovirus RNA is extremely long—over 700 nucleotides—and highly structured. This region of the viral genome is called an internal ribosome entry site (IRES). This region consists of many secondary structures and 3 or 4 domains. Domain 3 is a self folding RNA element that contains conserved structural motifs in various stable stem loops linked by two four-way junctions. As IRES consists of many domains, these domains themselves consist of many loops that contribute to modified translation without a 5’ end cap by hijacking ribosomes. The interaction loop of domain 3 is known as GNRA tetraloop. The residues of adenosines A180 and A181 in the GUAA tetraloop form hydrogen bonds via non canonical base pairing interactions with the base pairs of the receptors C230/G242 and G231/C241, respectively. [13] Genetic mutations in this region prevent viral protein production. [14] [15] [16] The first IRES to be discovered was found in poliovirus RNA. [17]

Poliovirus mRNA is translated as one long polypeptide. This polypeptide is then autocleaved by internal proteases into about 10 individual viral proteins. Not all cleavages occur with the same efficiency. Therefore, the amounts of proteins produced by the polypeptide cleavage vary: for example, smaller amounts of 3Dpol are produced than those of capsid proteins, VP1–4. [18] : 165  [19] These individual viral proteins are: [3] [20]

The genomic structure of poliovirus type 1 Poliovirus genome.png
The genomic structure of poliovirus type 1

After translation, transcription and genome replication which involve a single process, synthesis of (+) RNA) is realized. For the infecting (+)RNA to be replicated, multiple copies of (−)RNA must be transcribed and then used as templates for (+)RNA synthesis. Replicative intermediates (RIs), which are an association of RNA molecules consisting of a template RNA and several growing RNAs of varying length, are seen in both the replication complexes for (−)RNAs and (+)RNAs. For synthesis of each negative-strand and positive-strand RNAs, VPg protein in the poliovirus works as a primer. RNA-dependent RNA polymerase of the poliovirus adds two uracil nucleotides (UU) to VPg protein utilizing the poly(A) tail at the 3′-end of the +ssRNA genome as a pattern for synthesis of the negative-strand antigenomic RNA. To initiate this −ssRNA synthesis, the tyrosine hydroxyl of VPg is needed. But for the initiation of positive strand RNA synthesis, CRE-dependent VPg uridylylation is needed. Which means that VPg is once more utilized as a primer however this time it adds the two uridine triphosphates using a cis-acting replication element (CRE) as a template. [22] [23]

The CRE of poliovirus is identified as an unachieved base-paired stem and a final loop consisting of 61 nt. The CRE is found in enteroviruses. It is a highly preserved secondary RNA structural element and bedded in the genome's polyprotein-coding region. The complex can be translocated to the 5' region of the genome that have no coding activity, at least 3.7-kb distant from the initial location. This process can occurs without negatively influencing activity. CRE copies do not influence replication negatively. Uridylylation process of VPg that takes place at CRE needs the presence of 3CDpro that is an RNA binding protein. It is attached to the CRE directly and specifically. Because of its presence VPg can bind the CRE properly and primary production proceeds without problems. [24]

Some of the (+) RNA molecules are used as templates for further (−) RNA synthesis, some function as mRNA, and some are destined to be the genomes of progeny virions. [18]

In the assembly of new virus particles (i.e. the packaging of progeny genome into a procapsid which can survive outside the host cell), including, respectively: [18] : 161, 165 

Fully assembled poliovirus leaves the confines of its host cell by lysis [25] 4 to 6 hours following initiation of infection in cultured mammalian cells. [26] The mechanism of viral release from the cell is unclear, [2] but each dying cell can release up to 10,000 polio virions. [26]

Drake demonstrated that poliovirus is able to undergo multiplicity reactivation. [27] That is, when polioviruses were irradiated with UV light and allowed to undergo multiple infections of host cells, viable progeny could be formed even at UV doses that inactivated the virus in single infections. Poliovirus can undergo genetic recombination when at least two viral genomes are present in the same host cell. Kirkegaard and Baltimore [28] presented evidence that RNA-dependent RNA polymerase (RdRP) catalyzes recombination by a copy choice mechanism in which the RdRP switches between (+)ssRNA templates during negative strand synthesis. Recombination in RNA viruses appears to be an adaptive mechanism for repairing genome damage. [29] [30]

Origin and serotypes

Poliovirus is structurally similar to other human enteroviruses (coxsackieviruses, echoviruses, and rhinoviruses), which also use immunoglobulin-like molecules to recognize and enter host cells. [6] Phylogenetic analysis of the RNA and protein sequences of poliovirus suggests that it may have evolved from a C-cluster Coxsackie A virus ancestor through a mutation in the capsid. [31] The distinct speciation of poliovirus probably occurred as a result of a change in cellular receptor specificity from intercellular adhesion molecule-1 (ICAM-1) (used by C-cluster Coxsackie A viruses) to CD155, leading to a change in pathogenicity and allowing the virus to infect nerve tissue.

The mutation rate in the virus is relatively high even for an RNA virus, with a synonymous substitution rate of 1.0 × 10−2 substitutions/site/year and a non-synonymous substitution rate of 3.0 × 10−4 substitutions/site/year. [32] Base distribution within the genome is not random; adenosine is less common than expected at the 5' end and higher at the 3' end. [33] Codon use is not random; codons ending in adenosine are favoured, and those ending in cytosine or guanine are avoided. Codon use differs between the three genotypes, and appears to be driven by mutation rather than selection. [34]

The three serotypes of poliovirus, PV-1, PV-2, and PV-3, each have a slightly different capsid protein. Capsid proteins define cellular receptor specificity and virus antigenicity. PV-1 is the most common form encountered in nature, but all three forms are extremely infectious. [35] As of March 2020, wild PV-1 is highly localized to regions in Pakistan and Afghanistan. Certification of the eradication of indigenous transmission of wild PV-2 occurred in September 2015, after last being detected in 1999, [36] and in October 2019 for wild PV-3 after last being detected in 2012. [37] However, circulating vaccine-derived poliovirus (variant poliovirus, cVDPV) of all three serotypes continues to circulate and cause paralysis, having been detected in 32 countries in 2023. [38]

Specific strains of each serotype are used to prepare vaccines against polio. Inactive polio vaccine is prepared by formalin inactivation of three wild, virulent reference strains: Mahoney or Brunenders (PV-1), MEF-1/Lansing (PV-2), and Saukett/Leon (PV-3). Oral polio vaccine contains live attenuated (weakened) strains of the three serotypes of poliovirus. Passaging the virus strains in monkey kidney epithelial cells introduces mutations in the viral IRES, and hinders (or attenuates) the ability of the virus to infect nerve tissue. [26]

Polioviruses were formerly classified as a distinct species belonging to the genus Enterovirus in the family Picornaviridae. In 2008, Poliovirus ceased to be recognized as a species, and the three serotypes were assigned to the species Human enterovirus C (later renamed Enterovirus C) in the genus Enterovirus in the family Picornaviridae. The type species of the genus Enterovirus was changed from Poliovirus to (Human) Enterovirus C. [39]

Pathogenesis

Electron micrograph of poliovirus Polio EM PHIL 1875 lores.PNG
Electron micrograph of poliovirus

The primary determinant of infection for any virus is its ability to enter a cell and produce additional infectious particles. The presence of CD155 is thought to define the animals and tissues that can be infected by poliovirus. CD155 is found (outside of laboratories) only on the cells of humans, higher primates, and Old World monkeys. Poliovirus is, however, strictly a human pathogen, and does not naturally infect any other species (although chimpanzees and Old World monkeys can be experimentally infected). [40]

The CD155 gene appears to have been subject to positive selection. [41] The protein has several domains of which domain D1 contains the polio virus binding site. Within this domain, 37 amino acids are responsible for binding the virus.

Poliovirus is an enterovirus. Infection occurs via the fecal–oral route, meaning that one ingests the virus and viral replication occurs in the gastrointestinal tract. [42] Virus is shed in the feces of infected individuals. In 95% of cases only a primary, transient presence of viremia (virus in the bloodstream) occurs, and the poliovirus infection is asymptomatic. In about 5% of cases, the virus spreads and replicates in other sites such as brown fat, reticuloendothelial tissue, and muscle. The sustained viral replication causes secondary viremia and leads to the development of minor symptoms such as fever, headache, and sore throat. [43] Paralytic poliomyelitis occurs in less than 1% of poliovirus infections. Paralytic disease occurs when the virus enters the central nervous system (CNS) and replicates in motor neurons within the spinal cord, brain stem, or motor cortex, resulting in the selective destruction of motor neurons leading to temporary or permanent paralysis. This is a very rare event in babies, who still have anti-poliovirus antibodies acquired from their mothers. [44] In rare cases, paralytic poliomyelitis leads to respiratory arrest and death. In cases of paralytic disease, muscle pain and spasms are frequently observed prior to onset of weakness and paralysis. Paralysis typically persists from days to weeks prior to recovery. [45]

In many respects, the neurological phase of infection is thought to be an accidental diversion of the normal gastrointestinal infection. [10] The mechanisms by which poliovirus enters the CNS are poorly understood. Three nonmutually exclusive hypotheses have been suggested to explain its entry. All theories require primary viremia. The first hypothesis predicts that virions pass directly from the blood into the central nervous system by crossing the blood–brain barrier independent of CD155. [46] A second hypothesis suggests that the virions are transported from peripheral tissues that have been bathed in the viremic blood, for example muscle tissue, to the spinal cord through nerve pathways via retrograde axonal transport. [47] [48] [49] A third hypothesis is that the virus is imported into the CNS via infected monocytes or macrophages. [4]

Poliomyelitis is a disease of the central nervous system. However, CD155 is believed to be present on the surface of most or all human cells. Therefore, receptor expression does not explain why poliovirus preferentially infects certain tissues. This suggests that tissue tropism is determined after cellular infection. Recent work has suggested that the type I interferon response (specifically that of interferon alpha and beta) is an important factor that defines which types of cells support poliovirus replication. [50] In mice expressing CD155 (through genetic engineering) but lacking the type I interferon receptor, poliovirus not only replicates in an expanded repertoire of tissue types, but these mice are also able to be infected orally with the virus. [51]

Immune system avoidance

CD155 molecules complexed with a poliovirus particle. Reconstructed image from cryo-electron microscopy. CD155 molecules complexed with a poliovirus particle.png
CD155 molecules complexed with a poliovirus particle. Reconstructed image from cryo-electron microscopy.

Poliovirus has two key mechanisms to evade the immune system. First, it can survive the highly acidic conditions of the stomach, allowing ingested viruses to infect the host and spread throughout the body via the lymphatic system. [3] Second, because it can replicate very quickly, the virus overwhelms the host's organs before an immune response can be mounted. [52] If detail is given at the attachment phase; poliovirus with canyons on the virion surface have virus attachment sites located in pockets at the canyon bases. The canyons are too narrow for access by antibodies, so the virus attachment sites are protected from the host's immune surveillance, while the remainder of the virion surface can mutate to avoid the host's immune response. [53]

Individuals who are exposed to poliovirus, either through infection or by immunization with polio vaccine, develop immunity. In immune individuals, antibodies against poliovirus are present in the tonsils and gastrointestinal tract (specifically IgA antibodies) and are able to block poliovirus replication; IgG and IgM antibodies against poliovirus can prevent the spread of the virus to motor neurons of the central nervous system. [26] Infection with one serotype of poliovirus does not provide immunity against the other serotypes; however, second attacks within the same individual are extremely rare. [54]

Eradication

This section is an excerpt from Polio eradication.[ edit ]
A child receives oral polio vaccine during a 2002 campaign to immunize children in India. Vaccination-polio-india.jpg
A child receives oral polio vaccine during a 2002 campaign to immunize children in India.
Poliovirus Polio.jpg
Poliovirus

Polio eradication, the goal of permanent global cessation of circulation of the poliovirus and hence elimination of the poliomyelitis (polio) it causes, is the aim of a multinational public health effort begun in 1988, led by the World Health Organization (WHO), the United Nations Children's Fund (UNICEF) and the Rotary Foundation. [55] These organizations, along with the U.S. Centers for Disease Control and Prevention (CDC) and The Gates Foundation, have spearheaded the campaign through the Global Polio Eradication Initiative (GPEI). Successful eradication of infectious diseases has been achieved twice before, with smallpox in humans [56] and rinderpest in ruminants. [57]

Prevention of disease spread is accomplished by vaccination. There are two kinds of polio vaccine—oral polio vaccine (OPV), which uses weakened poliovirus, and inactivated polio vaccine (IPV), which is injected. OPV is less expensive and easier to administer, and can spread immunity beyond the person vaccinated, creating contact immunity. It has been the predominant vaccine used. However, under conditions of long-term vaccine virus circulation in under-vaccinated populations, mutations can reactivate the virus to produce a polio-inducing strain, while OPV can also, in rare circumstances, induce polio or persistent asymptomatic infection in vaccinated individuals, particularly those who are immunodeficient. IPV, being inactivated, does not carry these risks, but does not induce contact immunity. IPV is more costly and the logistics of its delivery are more challenging.

Nigeria is the latest country to have officially stopped endemic transmission of wild poliovirus, with its last reported case in 2016. [58] Of the three strains of WPV, the last recorded wild case caused by type 2 (WPV2) was in 1999, and WPV2 was declared eradicated in 2015. Type 3 (WPV3) is last known to have caused polio in 2012, and was declared eradicated in 2019. [59] All wild-virus cases since that date have been due to type 1 (WPV1). [60]

As of August 2024, Afghanistan and Pakistan are the only two countries where the disease is still classified as endemic. [61] [62] Recent polio cases arise from two sources, the original "wild" poliovirus (WPV), and the much more prevalent mutated oral vaccine strains, known as circulating vaccine-derived poliovirus (cVDPV) or variant poliovirus. Vaccines against each of the three wild strains of polio have given rise to strains of cVDPV, with cVDPV2 being most prominent. cVDPV caused 524 confirmed paralytic polio cases worldwide in 2023, and was detected in 32 countries. [60]

Research

Transgenic mice

Although humans are the only known natural hosts of poliovirus, monkeys can be experimentally infected and they have long been used to study poliovirus. In 1990–91, a small animal model of poliomyelitis was developed by two laboratories. Mice were engineered to express a human receptor to poliovirus (hPVR). [63] [64]

Unlike normal mice, transgenic poliovirus receptor (TgPVR) mice are susceptible to poliovirus injected intravenously or intramuscularly, and when injected directly into the spinal cord or the brain. [65] Upon infection, TgPVR mice show signs of paralysis that resemble those of poliomyelitis in humans and monkeys, and the central nervous systems of paralyzed mice are histocytochemically similar to those of humans and monkeys. This mouse model of human poliovirus infection has proven to be an invaluable tool in understanding poliovirus biology and pathogenicity. [66]

Three distinct types of TgPVR mice have been well studied: [67]

The development of the TgPVR mouse has had a profound effect on oral poliovirus vaccine (OPV) production. Previously, monitoring the safety of OPV had to be performed using monkeys, because only primates are susceptible to the virus. In 1999, the World Health Organization approved the use of the TgPVR mouse as an alternative method of assessing the effectiveness of the vaccine against poliovirus type-3. In 2000, the mouse model was approved for tests of vaccines against type-1 and type-2 poliovirus. [69]

Genetic modification

A modification of the poliovirus, called PVSRIPO, was tested in early clinical trials as a possible treatment for cancer. [70] As of September 2022, a number of clinical trials are under way. [71] [72]

A drawback of the attenuated virus used in the Sabin oral polio vaccine is its potential to cause vaccine-associated paralytic poliomyelitis (VAPP) in approximately one individual per every 2.7 million doses administered. [73] In addition, the live virus can also circulate in under-vaccinated populations (circulating vaccine-derived poliovirus, cVDPV) and over time can revert to a neurovirulent form causing paralytic polio. [73] Researchers have developed a poliovirus type 2 vaccine strain that is genetically more stable and less likely to regain virulence than the original Sabin2 strain, with three key genetic modifications. [74] The vaccine derived from this strain, novel oral polio virus type 2 (nOPV2), was granted emergency licencing in 2021, and subsequently full licensure in December 2023. [75] Genetically stabilsed vaccines targeting poliovirus types 1 and 3 are in development, with the intention that these will eventually completely replace the Sabin vaccines. [76]

History

Discovery

Poliovirus was first isolated in 1909 by Karl Landsteiner and Erwin Popper. [35] The structure of the virus was first elucidated in 1958 using X-ray diffraction by a team at Birkbeck College led by Rosalind Franklin, [77] [78] showing the polio virus to have icosahedral symmetry. [79]

Genome

In 1981, the poliovirus genome was published by two different teams of researchers: by Vincent Racaniello and David Baltimore at MIT [80] and by Naomi Kitamura and Eckard Wimmer at Stony Brook University. [81]

Structure

The three-dimensional structure of poliovirus was determined in 1985 by James Hogle at Scripps Research Institute using X-ray crystallography. [82]

Cloning and synthesis

Model of poliovirus-binding CD155 (shown in purple) Poliovirus binding receptor 1DGI.png
Model of poliovirus-binding CD155 (shown in purple)

In 1981, Racaniello and Baltimore used recombinant DNA technology to generate the first infectious clone of an animal RNA virus, poliovirus. DNA encoding the RNA genome of poliovirus was introduced into cultured mammalian cells and infectious poliovirus was produced. [83] Creation of the infectious clone propelled understanding of poliovirus biology, and has become a standard technology used to study many other viruses.

In 2002, Eckard Wimmer's group at Stony Brook University succeeded in synthesizing poliovirus from its chemical code, producing the world's first synthetic virus. [84] Scientists first converted poliovirus's published RNA sequence, 7741 bases long, into a DNA sequence, as DNA was easier to synthesize. Short fragments of this DNA sequence were obtained by mail-order, and assembled. The complete viral genome was then assembled by a gene synthesis company. Nineteen markers were incorporated into the synthesized DNA, so that it could be distinguished from natural poliovirus. Enzymes were used to convert the DNA back into RNA, its natural state. Other enzymes were then used to translate the RNA into a polypeptide, producing functional viral particle. This whole painstaking process took two years. The newly minted synthetic virus was injected into PVR transgenic mice, to determine if the synthetic version was able to cause disease. The synthetic virus was able to replicate, infect, and cause paralysis or death in mice. However, the synthetic version was between 1,000 and 10,000 times weaker than the original virus, probably due to one of the added markers. [85]

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Poliomyelitis, commonly shortened to polio, is an infectious disease caused by the poliovirus. Approximately 75% of cases are asymptomatic; mild symptoms which can occur include sore throat and fever; in a proportion of cases more severe symptoms develop such as headache, neck stiffness, and paresthesia. These symptoms usually pass within one or two weeks. A less common symptom is permanent paralysis, and possible death in extreme cases. Years after recovery, post-polio syndrome may occur, with a slow development of muscle weakness similar to what the person had during the initial infection.

Coxsackie B4 virus are enteroviruses that belong to the Picornaviridae family. These viruses can be found worldwide. They are positive-sense, single-stranded, non-enveloped RNA viruses with icosahedral geometry. Coxsackieviruses have two groups, A and B, each associated with different diseases. Coxsackievirus group A is known for causing hand-foot-and-mouth diseases while Group B, which contains six serotypes, can cause a varying range of symptoms like gastrointestinal distress myocarditis. Coxsackievirus B4 has a cell tropism for natural killer cells and pancreatic islet cells. Infection can lead to beta cell apoptosis which increases the risk of insulitis.

<span class="mw-page-title-main">Coxsackievirus</span> Virus that causes digestive upset and sometimes heart damage

Coxsackieviruses are a few related enteroviruses that belong to the Picornaviridae family of nonenveloped, linear, positive-sense single-stranded RNA viruses, as well as its genus Enterovirus, which also includes poliovirus and echovirus. Enteroviruses are among the most common and important human pathogens, and ordinarily its members are transmitted by the fecal–oral route. Coxsackieviruses share many characteristics with poliovirus. With control of poliovirus infections in much of the world, more attention has been focused on understanding the nonpolio enteroviruses such as coxsackievirus.

<span class="mw-page-title-main">Sedoreoviridae</span> Family of viruses

Sedoreoviridae is a family of double-stranded RNA viruses. Member viruses have a wide host range, including vertebrates, invertebrates, plants, protists and fungi. They lack lipid envelopes and package their segmented genome within multi-layered capsids. Lack of a lipid envelope has allowed three-dimensional structures of these large complex viruses to be obtained, revealing a structural and likely evolutionary relationship to the cystovirus family of bacteriophage. There are currently 97 species in this family, divided among 15 genera in two subfamilies. Reoviruses can affect the gastrointestinal system and respiratory tract. The name "reo-" is an acronym for "respiratory enteric orphan" viruses. The term "orphan virus" refers to the fact that some of these viruses have been observed not associated with any known disease. Even though viruses in the family Reoviridae have more recently been identified with various diseases, the original name is still used.

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<span class="mw-page-title-main">Picornavirus</span> Family of viruses

Picornaviruses are a group of related nonenveloped RNA viruses which infect vertebrates including fish, mammals, and birds. They are viruses that represent a large family of small, positive-sense, single-stranded RNA viruses with a 30 nm icosahedral capsid. The viruses in this family can cause a range of diseases including the common cold, poliomyelitis, meningitis, hepatitis, and paralysis.

<span class="mw-page-title-main">SV40</span> Species of virus

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<span class="mw-page-title-main">Measles virus</span> Species of virus

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<i>Enterovirus</i> Genus of viruses

Enterovirus is a genus of positive-sense single-stranded RNA viruses associated with several human and mammalian diseases. Enteroviruses are named by their transmission-route through the intestine.

Viral pathogenesis is the study of the process and mechanisms by which viruses cause diseases in their target hosts, often at the cellular or molecular level. It is a specialized field of study in virology.

VPg is a protein that is covalently attached to the 5′ end of positive strand viral RNA and acts as a primer during RNA synthesis in a variety of virus families including Picornaviridae, Potyviridae, Astroviridae and Caliciviridae. There are some studies showing that a possible VPg protein is also present in astroviridae, however, experimental evidence for this has not yet been provided and requires further study. The primer activity of VPg occurs when the protein becomes uridylated, providing a free hydroxyl that can be extended by the virally encoded RNA-dependent RNA polymerase. For some virus families, VPg also has a role in translation initiation by acting like a 5' mRNA cap.

<i>Aphthovirus</i> Genus of viruses

Aphthovirus is a viral genus of the family Picornaviridae. Aphthoviruses infect split-hooved animals, and include the causative agent of foot-and-mouth disease, Foot-and-mouth disease virus (FMDV). There are seven FMDV serotypes: A, O, C, SAT 1, SAT 2, SAT 3 and Asia 1, and four non-FMDV serotypes belonging to three additional species Bovine rhinitis A virus (BRAV), Bovine rhinitis B virus (BRBV) and Equine rhinitis A virus (ERAV).

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<span class="mw-page-title-main">CD155</span> Protein found in humans

CD155, also known as the poliovirus receptor, is a protein that in humans is encoded by the PVR gene. It is a transmembrane protein that is involved in forming junctions between neighboring cells. It is also the molecule that poliovirus uses to enter cells. The gene is specific to the primates.

<span class="mw-page-title-main">RNA-dependent RNA polymerase</span> Enzyme that synthesizes RNA from an RNA template

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<span class="mw-page-title-main">Vincent Racaniello</span> American biologist

Vincent R. Racaniello is a Higgins Professor in the Department of Microbiology and Immunology at Columbia University's College of Physicians and Surgeons. He is a co-author of a textbook on virology, Principles of Virology.

Eckard Wimmer is a German American virologist, organic chemist and distinguished professor of molecular genetics and microbiology at Stony Brook University. He is best known for his seminal work on the molecular biology of poliovirus and the first chemical synthesis of a viral genome capable of infection and subsequent production of live viruses.

<span class="mw-page-title-main">Picornain 3C</span>

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Polioencephalitis is a viral infection of the brain, causing inflammation within the grey matter of the brain stem. The virus has an affinity for neuronal cell bodies and has been found to affect mostly the midbrain, pons, medulla and cerebellum of most infected patients. The infection can reach up through the thalamus and hypothalamus and possibly reach the cerebral hemispheres. The infection is caused by the poliomyelitis virus which is a single-stranded, positive sense RNA virus surrounded by a non-enveloped capsid. Humans are the only known natural hosts of this virus. The disease has been eliminated from the U.S. since the mid-twentieth century, but is still found in certain areas of the world such as Africa.

References

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