The neuropathology observed in wild-type mice inoculated with human poliovirus mirrors human paralytic poliomyelitis

Ford, Dayton J.; Ropka, Stacie L.; Collins, George H.; Jubelt, Burk

doi:10.1006/mpat.2002.0512

Cited by 16 publications

(7 citation statements)

References 42 publications

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“…inoculation of PV/HRV2 chimeras. However, detailed neuropathological analysis indicates that CD155 tg mouse model may not accurately reflect the human poliomyelitis [Ford et al, 2002]. Moreover, the level of expression of CD155 on some tissues of transgenic mice is different than those observed on the human tissues [Iwasaki et al, 2002].…”

Section: Discussionmentioning

confidence: 94%

Growth phenotypes and biosafety profiles in poliovirus‐receptor transgenic mice of recombinant oncolytic polio/human rhinoviruses

Cello

Toyoda

DeJesus

et al. 2007

Journal of Medical Virology

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The use of oncolytic recombinant polioviruses has an important therapeutic potential in the treatment of human gliomas. This study was carried out to assess parameters of the utility of the oncolytic poliovirus/human rhinovirus type 2 chimeras (PV/HRV2). The prototype PV/HRV2 chimera was constructed containing the complete genome of wild-type PV type 1 (Mahoney) [PV1(M)] in which the cognate IRES was replaced with that of HRV2 [called PV1(RIPO)]. A derivative of PV1(RIPO) is PV1(RIPOS) in which the capsid coding region (P1) was replaced with the capsid-coding region of the PV type 1 (Sabin) [PV1(S)] vaccine strain. In addition, a third PV/HRV2 chimera was constructed containing the complete genome of PV1(S) in which the cognate IRES was replaced with that of HRV2 [termed PVS(RIPO)]. To analyze the growth phenotypes of PV/HRV2 recombinants [PV1(RIPO), PV1(RIPOS), PVS(RIPO)], one-step growth experiments were performed in four human cell lines at three different temperatures. To address the safety profile, PVS(RIPO) was injected into the brain of CD155 tg mice at the dose 10(7) PFU. Then, clinical signs, persistence of the virus in the CNS and genetic stability of PVS(RIPO) replicating in the CNS were evaluated. The data obtained in the present study suggest (i) a correlation between temperature-sensitive (ts) phenotype in both neuronal and non-neuronal cell lines and neuroattenuation in experimental animals, (ii) that PVS (RIPO) is genetically stable on replication in the CNS of poliovirus-susceptible mice. These findings highlight the safety of intracerebral inoculation of PVS(RIPO) for the treatment of human glioma.

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Section: Discussionmentioning

confidence: 94%

Growth phenotypes and biosafety profiles in poliovirus‐receptor transgenic mice of recombinant oncolytic polio/human rhinoviruses

Cello

Toyoda

DeJesus

et al. 2007

Journal of Medical Virology

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“…In the brain, this includes large motor neurons in the precentral gyrus (Betz cells) and neurons of the thalamus and hypothalamus (Bodian 1972;Ford et al 2002). In the brainstem, motor nuclei (facial, hypoglossal, and nucleus (Bodian 1972;Ford et al 2002). In the spinal cord, intermediate, posterior horn, and even dorsal root ganglia may be infected (Bodian 1972).…”

Section: Pathogenesis and Pathologymentioning

confidence: 97%

“…Neurons other than spinal cord anterior horn cells may also be infected. In the brain, this includes large motor neurons in the precentral gyrus (Betz cells) and neurons of the thalamus and hypothalamus (Bodian 1972;Ford et al 2002). In the brainstem, motor nuclei (facial, hypoglossal, and nucleus (Bodian 1972;Ford et al 2002).…”

Section: Pathogenesis and Pathologymentioning

confidence: 98%

“…Viremia precedes and appears to be required for CNS invasion (Nathanson and Bodian 1962). After the viremia, it is unclear if virus enters the CNS via areas where the blood-brain barrier is defective, such as the area postrema (Bodian 1954) or via seeding the neuromuscular junction followed by retrograde axonal transport to the neuronal cell body (Ren and Racaniello 1992;Ford et al 2002). It is thought that coxsackieviruses and echoviruses enter the CSF through the choroid plexus from the viremia.…”

Section: Pathogenesis and Pathologymentioning

confidence: 98%

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Enterovirus Infections

Jubelt¹

2012

Viral Infections of the Human Nervous System

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The human enteroviruses (EV) comprise one group of the picornavirus family. The best known members are the polioviruses (PV), coxsackieviruses, and echoviruses. They replicate in the oropharynx and gastrointestinal (GI) tract and are primarily spread by fecal-hand-oral contamination. With systemic invasion nonspecific febrile illness occurs as well as specific syndromes (rashes, hand-footand-mouth disease, herpangina, pleurodynia, myocarditis/pericarditis, and conjunctivitis). With systemic replication a high level viremia may result in central nervous system (CNS) invasion. EV activity can be endemic in warm climates or epidemic in temperate climates. In temperate climates, because of improved hygiene, newborns were not exposed to EV until they were older, resulting in large epidemics of poliomyelitis, which were finally curtailed with the killed PV vaccines in the 1950s and the live oral PV vaccines in the 1960s. Today, "aseptic" meningitis is the most common neurologic syndrome caused by EV. EV are also the most common cause of viral meningitis. Other EV neurologic syndromes include encephalitis, rhombencephalitis, paralytic disease, persistent infections, and the severe group B coxsackievirus fatal systemic infections of neonates. Diagnostic clues can come from epidemics, systemic manifestations, household infections, the cerebrospinal picture, and the neurologic syndrome. However, definite diagnosis depends on laboratory methods, primarily nucleic acid amplification. Treatment of acute infections is supportive. Preventative methods include good hygiene and aggressive polio vaccination programs.

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“…Another line of research has also raised some interesting questions: By injection of PV into the normal brain, mutant PVs have been recovered that show a selective infection and destruction of normal mouse motor neurons in the absence of PVR binding (Ford et al,2002; Jubelt et al,1980;1980a), or more generalized infection of the CNS with mouse-brain derived mutant PV (Grommeier et al1995). A single six amino acid sequence in the VP1 capsid protein may enable PV to infect non-PVR mouse motor neurons (Martin et al,1988; Murray et al, 1988).…”

Section: Cellular Tropism Of Pvmentioning

confidence: 99%

Polio, Still Lurking in the Shadows

Pol

2013

J. Neurosci.

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The neuropathology observed in wild-type mice inoculated with human poliovirus mirrors human paralytic poliomyelitis

Cited by 16 publications

References 42 publications

Growth phenotypes and biosafety profiles in poliovirus‐receptor transgenic mice of recombinant oncolytic polio/human rhinoviruses

Growth phenotypes and biosafety profiles in poliovirus‐receptor transgenic mice of recombinant oncolytic polio/human rhinoviruses

Enterovirus Infections

Polio, Still Lurking in the Shadows

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