POLIOVIRUS
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(Redirected from Polio virus)
'Poliovirus' is a human enterovirus in the family of Picornaviridae, and the causative agent in poliomyelitis. Sherris Medical Microbiology, Ryan KJ, Ray CG (editors), , , McGraw Hill, 2004, It is a small RNA virus (ribonucleic acid), about 300 Ã…ngström in diameter, with a single-stranded positive-sense RNA genome that is about 7500 bases long. Poliovirus cell entry: common structural themes in viral cell entry pathways, Hogle J, , , Annu Rev Microbiol, 2002 Poliovirus was isolated in 1908 by Karl Landsteiner and Erwin Popper. A History of Poliomyelitis, Paul JR, , , Yale University Press, 1971, In 1981, the poliovirus genome was published by two different teams of researchers, one at MIT and the other at the State University of New York, Stony Brook. Primary structure, gene organization and polypeptide expression of poliovirus RNA, Kitamura N, Semler B, Rothberg P, ''et al'', , , Nature, 1981 Because of its short genome and its simple composition—only RNA and a non-enveloped icosahedral protein coat that encapsulates it—poliovirus is widely regarded as the simplest significant virus. The machinery of life, Goodsell DS, , , Copernicus, 1998,
There are three serotypes of poliovirus, ''PV1'' (Mahoney), ''PV2'' (Lansing), and ''PV3'' (Leon); each with a slightly different capsid protein. Capsid proteins define cellular receptor specificity and virus antigenicity. ''PV1'' is the most common form encountered in nature, however all three forms are extremely infectious.
All three forms of poliovirus are structurally similar to other human enteroviruses, coxsackieviruses, echoviruses, and to human rhinoviruses, which also use immunoglobulin-like molecules to recognize and enter host cells. Phylogenetic analysis of the RNA and protein sequences of poliovirus suggests that PV may have evolved from a C-cluster coxsackie A virus ancestor, arising through a mutation within the capsid.[1] The distinct speciation of poliovirus probably occurred as a result of 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 nervous tissue.
Poliovirus infects human cells by binding to an immunoglobulin-like receptor — CD155, also known as the ''poliovirus receptor'' (PVR) — on the cell surface. Complexes of poliovirus serotypes with their common cellular receptor, CD155, He Y, Mueller S, Chipman P, ''et al'', , , J Virol, 2003 The precise mechanism poliovirus uses to enter the host cell has not been firmly established. Picornaviruses: The Enteroviruses: Polioviruses ''in:'' Baron's Medical Microbiology ''(Baron S ''et al'', eds.), , , , Univ of Texas Medical Branch, 1996, It may be that binding to CD155 triggers a conformational change in the virus which allows it to attach to the host cell membrane, followed by the formation of a pore in the membrane through which the viral RNA is then “injected†into the host cell cytoplasm. Another hypothesis is that the virus is taken up via receptor-mediated endocytosis. Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event, Mueller S, Wimmer E, Cello J, , , Virus Res, 2005 By either mechanism the poliovirus entry strategy is very inefficient; it is able to initiate an infection only about 1% of the time.Charles Chan and Roberto Neisa. "Poliomyelitis". Brown University.
Once inside the cell, the viral RNA acts like the host messenger RNA and, uses the host's own machinery to copy itself. The virus initiates replication of new viruses via a highly structured portion of the viral genome that binds to the host translational machinery. This portion of the poliovirus genome is known as the internal ribosome entry site (IRES). The IRES is required for poliovirus replication. The genome of poliovirus is only large enough to encode about 10 genes. These genes encode for a small number of viral proteins including:
★ ''3Dpol'', an RNA dependent RNA polymerase, which allows polio's RNA genome to be copied within the host cell. The entire polio genome is copied into in one long strand of protein.
★ ''2Apro'' and ''3Cpro/3CDpro'', proteases, that cleave the long strand of viral protein into functional products.
★ A small protein (VPg) tags the virus's RNA, so that it can be differentiated from host RNA.
★ Several proteins that inhibit the host cell's normal synthesis of proteins.
★ Four capsid proteins, VP0, VP1 VP3 and VP4.
The assembly of new virus particles, (i.e. the packaging of progeny genomes into capsids which can survive outside the host cell) is poorly understood. Fully assembled poliovirus leaves the confines of its host cell when the cell dies, which occurs 4 to 6 hours following infection. Vaccine-derived polioviruses and the endgame strategy for global polio eradication, Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M, , , Annu Rev Microbiol, 2005 The mechanism of viral release from the cell is unclear, but each dying cell can release as many as 10,000 polio virions.
Poliovirus infection is limited by expression of the CD155 receptor, which is found only on the cells of humans, higher primates, and Old World monkeys. Poliovirus is strictly a human pathogen, however, and it does not naturally infect any other species.[2]
Typically, poliovirus infection involves replication of the virus within the gastrointestinal tract and subsequent shedding of the virus in feces. In 95% of cases only primary, transient presence of the virus in the bloodstream occurs (called a viremia) and the poliovirus infection is asymptomatic. In about 5% of cases, the virus spreads, and replicates in other sites such as brown fat, the reticuloendothelial tissues, and muscle. This sustained replication causes a secondary viremia, and leads to the development of minor symptoms such as fever, headache and sore throat.[3]
In about 1-2% of poliovirus infections 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, and leading to either temporary or permanent paralysis and, in rare cases, to respiratory arrest and death. In many respects the neurological phase of infection is thought to be an accidental diversion of the normal gastrointestinal infection. The mechanisms by which poliovirus spreads to the CNS are poorly understood, two theories, however, have been suggested to explain the viral diversion.
The first hypothesis is that the virus passes directly from the blood into the central nervous system by crossing the blood brain barrier, without binding to its cellular receptor (CD155).[4] The second hypothesis suggests that the virus is transported from the muscle to the spinal cord through nerve pathways by retrograde axonal transport.[5] Both theories require that the virus be present in the blood (viremia), and it has been demonstrated that poliovirus can bind to and replicate within primary human monocytes in the blood,[6] which may then be involved in spreading the virus from the sites of primary infection (the gut) into the circulation, and potentially to the CNS.
Poliovirus uses two key mechanisms to evade the immune system. First, it is capable of surviving the highly acidic conditions of the gastrointestinal tract, allowing the virus to infect the host and spread throughout the body via the lymphatic system. Second, because it can replicate very rapidly - the virus overwhelms the host organs before an immune response can be mounted. One hundred years of poliovirus pathogenesis, Racaniello V, , , Virology, 2006
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. Infection with one serotype of poliovirus does not provide immunity against the other serotypes, however second attacks within the same individual are extremely rare.
Poliovirus is one of the most well-characterized viruses. 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 mouse model of polio was developed when two laboratories established lines of mice engineered to express a human receptor to poliovirus (hPVR).[7][8]
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.[9] 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.[10]
Three distinct types of TgPVR mice have been well studied:[11]
★ In TgPVR1 mice the transgene encoding the human PVR was incorporated into mouse chromosome 4. These mice express the highest levels of the transgene and the highest sensitivity to poliovirus. TgPVR1 mice are susceptible to poliovirus through the intraspinal, intracerebral, intramuscular, and intravenous pathways, but not through the oral route.
★ TgPVR21 mice have incorporated the human PVR at chromosome 13. These mice are less susceptible to poliovirus infection through the intracerebral route, possibly because they express decreased levels of hPVR. TgPVR21 mice have been shown to be susceptible to poliovirus infection through intranasal inoculation, and may be useful as a mucosal infection model.[12]
★ In TgPVR5 mice the human transgene is located on chromosome 12. These mice exhibit the lowest levels of hPVR expression and are the least susceptible to poliovirus infection.
★ Recently a forth TgPVR mouse model was developed. These "cPVR" mice, carry hPVR cDNA, driven by a β-actin promoter, and have proven susceptible to poliovirus through intracerebral, intramuscular, and intranasal routes. In addition, these mice are capable of developing the bulbar form of polio after intranasal inoculation.
The development of the TgPVR mouse has also 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.[13]
In 2002 researchers from SUNY Stony Brook succeeded in synthesizing poliovirus from its chemical code, producing the world's first synthetic virus.[14] Using the published genetic code, the scientists first converted poliovirus's RNA sequence into a DNA sequence, and short fragments of the DNA sequence were assembled. The complete virus 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.
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 less lethal than the original virus.[15]
1. Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication, Jiang P, Faase JA, Toyoda H, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 2007
2. Recruitment of nectin-3 to cell-cell junctions through trans-heterophilic interaction with CD155, a vitronectin and poliovirus receptor that localizes to alpha(v)beta3 integrin-containing membrane microdomains, Mueller S, Wimmer E, , , J Biol Chem, 2003
3. Pathogenesis of poliomyelitis; reappraisal in the light of new data, Sabin A, , , Science, 1956
4. Efficient delivery of circulating poliovirus to the central nervous system independently of poliovirus receptor, Yang W, Terasaki T, Shiroki K, ''et al'', , , Virology, 1997
5. Poliovirus spreads from muscle to the central nervous system by neural pathways, Ren R, Racaniello V, , , J Infect Dis, 1992
6. Hematopoietic cells from CD155-transgenic mice express CD155 and support poliovirus replication ex vivo, Freistadt M, Eberle K, , , Microb Pathog, 2000
7. Transgenic mice expressing a human poliovirus receptor: a new model for poliomyelitis, Ren RB, Costantini F, Gorgacz EJ, Lee JJ, Racaniello VR, , , Cell, 1990
8. Transgenic mice susceptible to poliovirus, Koike S, Taya C, Kurata T, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 1991
9. Transgenic mice carrying the human poliovirus receptor: new animal models for study of poliovirus neurovirulence, Horie H, Koike S, Kurata T, ''et al'', , , J. Virol., 1994
10. Recent insights into poliovirus pathogenesis, Ohka S, Nomoto A, , , Trends Microbiol., 2001
11. Characterization of three different transgenic mouse lines that carry human poliovirus receptor gene--influence of the transgene expression on pathogenesis, Koike S, Taya C, Aoki J, ''et al'', , , Arch. Virol., 1994
12. A poliomyelitis model through mucosal infection in transgenic mice bearing human poliovirus receptor, TgPVR21, Nagata N, Iwasaki T, Ami Y, ''et al'', , , Virology, 2004
13. Transgenic mice as an alternative to monkeys for neurovirulence testing of live oral poliovirus vaccine: validation by a WHO collaborative study, Dragunsky E, Nomura T, Karpinski K, ''et al'', , , Bull. World Health Organ., 2003
14. Chemical synthesis of poliovirus cDNA: generation of infectious virus in the absence of natural template, Cello J, Paul AV, Wimmer E, , , Science, 2002
15. Virology. Active poliovirus baked from scratch, Couzin J, , , Science, 2002
★ ICTVdb virus classification
'Poliovirus' is a human enterovirus in the family of Picornaviridae, and the causative agent in poliomyelitis. Sherris Medical Microbiology, Ryan KJ, Ray CG (editors), , , McGraw Hill, 2004, It is a small RNA virus (ribonucleic acid), about 300 Ã…ngström in diameter, with a single-stranded positive-sense RNA genome that is about 7500 bases long. Poliovirus cell entry: common structural themes in viral cell entry pathways, Hogle J, , , Annu Rev Microbiol, 2002 Poliovirus was isolated in 1908 by Karl Landsteiner and Erwin Popper. A History of Poliomyelitis, Paul JR, , , Yale University Press, 1971, In 1981, the poliovirus genome was published by two different teams of researchers, one at MIT and the other at the State University of New York, Stony Brook. Primary structure, gene organization and polypeptide expression of poliovirus RNA, Kitamura N, Semler B, Rothberg P, ''et al'', , , Nature, 1981 Because of its short genome and its simple composition—only RNA and a non-enveloped icosahedral protein coat that encapsulates it—poliovirus is widely regarded as the simplest significant virus. The machinery of life, Goodsell DS, , , Copernicus, 1998,
| Contents |
| Origin and serotypes |
| Life cycle |
| Pathogenesis |
| Immune system avoidance |
| PVR transgenic mouse |
| Artificial synthesis |
| References |
| External links |
Origin and serotypes
There are three serotypes of poliovirus, ''PV1'' (Mahoney), ''PV2'' (Lansing), and ''PV3'' (Leon); each with a slightly different capsid protein. Capsid proteins define cellular receptor specificity and virus antigenicity. ''PV1'' is the most common form encountered in nature, however all three forms are extremely infectious.
All three forms of poliovirus are structurally similar to other human enteroviruses, coxsackieviruses, echoviruses, and to human rhinoviruses, which also use immunoglobulin-like molecules to recognize and enter host cells. Phylogenetic analysis of the RNA and protein sequences of poliovirus suggests that PV may have evolved from a C-cluster coxsackie A virus ancestor, arising through a mutation within the capsid.[1] The distinct speciation of poliovirus probably occurred as a result of 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 nervous tissue.
Life cycle
Poliovirus infects human cells by binding to an immunoglobulin-like receptor — CD155, also known as the ''poliovirus receptor'' (PVR) — on the cell surface. Complexes of poliovirus serotypes with their common cellular receptor, CD155, He Y, Mueller S, Chipman P, ''et al'', , , J Virol, 2003 The precise mechanism poliovirus uses to enter the host cell has not been firmly established. Picornaviruses: The Enteroviruses: Polioviruses ''in:'' Baron's Medical Microbiology ''(Baron S ''et al'', eds.), , , , Univ of Texas Medical Branch, 1996, It may be that binding to CD155 triggers a conformational change in the virus which allows it to attach to the host cell membrane, followed by the formation of a pore in the membrane through which the viral RNA is then “injected†into the host cell cytoplasm. Another hypothesis is that the virus is taken up via receptor-mediated endocytosis. Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event, Mueller S, Wimmer E, Cello J, , , Virus Res, 2005 By either mechanism the poliovirus entry strategy is very inefficient; it is able to initiate an infection only about 1% of the time.Charles Chan and Roberto Neisa. "Poliomyelitis". Brown University.
The structural appearance of Poliovirus.
Once inside the cell, the viral RNA acts like the host messenger RNA and, uses the host's own machinery to copy itself. The virus initiates replication of new viruses via a highly structured portion of the viral genome that binds to the host translational machinery. This portion of the poliovirus genome is known as the internal ribosome entry site (IRES). The IRES is required for poliovirus replication. The genome of poliovirus is only large enough to encode about 10 genes. These genes encode for a small number of viral proteins including:
★ ''3Dpol'', an RNA dependent RNA polymerase, which allows polio's RNA genome to be copied within the host cell. The entire polio genome is copied into in one long strand of protein.
★ ''2Apro'' and ''3Cpro/3CDpro'', proteases, that cleave the long strand of viral protein into functional products.
★ A small protein (VPg) tags the virus's RNA, so that it can be differentiated from host RNA.
★ Several proteins that inhibit the host cell's normal synthesis of proteins.
★ Four capsid proteins, VP0, VP1 VP3 and VP4.
The assembly of new virus particles, (i.e. the packaging of progeny genomes into capsids which can survive outside the host cell) is poorly understood. Fully assembled poliovirus leaves the confines of its host cell when the cell dies, which occurs 4 to 6 hours following infection. Vaccine-derived polioviruses and the endgame strategy for global polio eradication, Kew O, Sutter R, de Gourville E, Dowdle W, Pallansch M, , , Annu Rev Microbiol, 2005 The mechanism of viral release from the cell is unclear, but each dying cell can release as many as 10,000 polio virions.
Pathogenesis
Electron micrograph of poliovirus.
Poliovirus infection is limited by expression of the CD155 receptor, which is found only on the cells of humans, higher primates, and Old World monkeys. Poliovirus is strictly a human pathogen, however, and it does not naturally infect any other species.[2]
Typically, poliovirus infection involves replication of the virus within the gastrointestinal tract and subsequent shedding of the virus in feces. In 95% of cases only primary, transient presence of the virus in the bloodstream occurs (called a viremia) and the poliovirus infection is asymptomatic. In about 5% of cases, the virus spreads, and replicates in other sites such as brown fat, the reticuloendothelial tissues, and muscle. This sustained replication causes a secondary viremia, and leads to the development of minor symptoms such as fever, headache and sore throat.[3]
In about 1-2% of poliovirus infections 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, and leading to either temporary or permanent paralysis and, in rare cases, to respiratory arrest and death. In many respects the neurological phase of infection is thought to be an accidental diversion of the normal gastrointestinal infection. The mechanisms by which poliovirus spreads to the CNS are poorly understood, two theories, however, have been suggested to explain the viral diversion.
The first hypothesis is that the virus passes directly from the blood into the central nervous system by crossing the blood brain barrier, without binding to its cellular receptor (CD155).[4] The second hypothesis suggests that the virus is transported from the muscle to the spinal cord through nerve pathways by retrograde axonal transport.[5] Both theories require that the virus be present in the blood (viremia), and it has been demonstrated that poliovirus can bind to and replicate within primary human monocytes in the blood,[6] which may then be involved in spreading the virus from the sites of primary infection (the gut) into the circulation, and potentially to the CNS.
Immune system avoidance
Poliovirus uses two key mechanisms to evade the immune system. First, it is capable of surviving the highly acidic conditions of the gastrointestinal tract, allowing the virus to infect the host and spread throughout the body via the lymphatic system. Second, because it can replicate very rapidly - the virus overwhelms the host organs before an immune response can be mounted. One hundred years of poliovirus pathogenesis, Racaniello V, , , Virology, 2006
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. Infection with one serotype of poliovirus does not provide immunity against the other serotypes, however second attacks within the same individual are extremely rare.
PVR transgenic mouse
Poliovirus is one of the most well-characterized viruses. 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 mouse model of polio was developed when two laboratories established lines of mice engineered to express a human receptor to poliovirus (hPVR).[7][8]
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.[9] 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.[10]
Three distinct types of TgPVR mice have been well studied:[11]
★ In TgPVR1 mice the transgene encoding the human PVR was incorporated into mouse chromosome 4. These mice express the highest levels of the transgene and the highest sensitivity to poliovirus. TgPVR1 mice are susceptible to poliovirus through the intraspinal, intracerebral, intramuscular, and intravenous pathways, but not through the oral route.
★ TgPVR21 mice have incorporated the human PVR at chromosome 13. These mice are less susceptible to poliovirus infection through the intracerebral route, possibly because they express decreased levels of hPVR. TgPVR21 mice have been shown to be susceptible to poliovirus infection through intranasal inoculation, and may be useful as a mucosal infection model.[12]
★ In TgPVR5 mice the human transgene is located on chromosome 12. These mice exhibit the lowest levels of hPVR expression and are the least susceptible to poliovirus infection.
★ Recently a forth TgPVR mouse model was developed. These "cPVR" mice, carry hPVR cDNA, driven by a β-actin promoter, and have proven susceptible to poliovirus through intracerebral, intramuscular, and intranasal routes. In addition, these mice are capable of developing the bulbar form of polio after intranasal inoculation.
The development of the TgPVR mouse has also 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.[13]
Artificial synthesis
In 2002 researchers from SUNY Stony Brook succeeded in synthesizing poliovirus from its chemical code, producing the world's first synthetic virus.[14] Using the published genetic code, the scientists first converted poliovirus's RNA sequence into a DNA sequence, and short fragments of the DNA sequence were assembled. The complete virus 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.
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 less lethal than the original virus.[15]
References
1. Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication, Jiang P, Faase JA, Toyoda H, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 2007
2. Recruitment of nectin-3 to cell-cell junctions through trans-heterophilic interaction with CD155, a vitronectin and poliovirus receptor that localizes to alpha(v)beta3 integrin-containing membrane microdomains, Mueller S, Wimmer E, , , J Biol Chem, 2003
3. Pathogenesis of poliomyelitis; reappraisal in the light of new data, Sabin A, , , Science, 1956
4. Efficient delivery of circulating poliovirus to the central nervous system independently of poliovirus receptor, Yang W, Terasaki T, Shiroki K, ''et al'', , , Virology, 1997
5. Poliovirus spreads from muscle to the central nervous system by neural pathways, Ren R, Racaniello V, , , J Infect Dis, 1992
6. Hematopoietic cells from CD155-transgenic mice express CD155 and support poliovirus replication ex vivo, Freistadt M, Eberle K, , , Microb Pathog, 2000
7. Transgenic mice expressing a human poliovirus receptor: a new model for poliomyelitis, Ren RB, Costantini F, Gorgacz EJ, Lee JJ, Racaniello VR, , , Cell, 1990
8. Transgenic mice susceptible to poliovirus, Koike S, Taya C, Kurata T, ''et al'', , , Proc. Natl. Acad. Sci. U.S.A., 1991
9. Transgenic mice carrying the human poliovirus receptor: new animal models for study of poliovirus neurovirulence, Horie H, Koike S, Kurata T, ''et al'', , , J. Virol., 1994
10. Recent insights into poliovirus pathogenesis, Ohka S, Nomoto A, , , Trends Microbiol., 2001
11. Characterization of three different transgenic mouse lines that carry human poliovirus receptor gene--influence of the transgene expression on pathogenesis, Koike S, Taya C, Aoki J, ''et al'', , , Arch. Virol., 1994
12. A poliomyelitis model through mucosal infection in transgenic mice bearing human poliovirus receptor, TgPVR21, Nagata N, Iwasaki T, Ami Y, ''et al'', , , Virology, 2004
13. Transgenic mice as an alternative to monkeys for neurovirulence testing of live oral poliovirus vaccine: validation by a WHO collaborative study, Dragunsky E, Nomura T, Karpinski K, ''et al'', , , Bull. World Health Organ., 2003
14. Chemical synthesis of poliovirus cDNA: generation of infectious virus in the absence of natural template, Cello J, Paul AV, Wimmer E, , , Science, 2002
15. Virology. Active poliovirus baked from scratch, Couzin J, , , Science, 2002
External links
★ ICTVdb virus classification
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