Immunofluorescent Study on the Pathogenesis of Oral Infection of Poliovirus in Monkey

Kanamitsu, Masatsugu; Kasamaki, Akiko; Ogawa, Mikio; Kasahara, Shoichi; Imamura, Masakatsu

doi:10.7883/yoken1952.20.175

Cited by 33 publications

(11 citation statements)

References 15 publications

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“…Indirect evidence of viral replication in motor neurons of primates and mice has already been reported by other authors, who detected poliovirus by electron microscopy (Bodian, 1964;Blinzinger et aL, 1969), by immunofluorescence (Kovacks et al, 1963;Kanamitsu et al, 1967;Jubelt et al, 1980a) or by immunocytochemical methods (Hashimoto et al, 1984;Dal Canto et al, 1986). Using quantification of silver grains in motor neurons of monkeys paralysed after infection with virulent PV-1/$1-39-C6, we have shown that the maximum number of viral genomes found in degenerating motor neurons was quite similar to the maximum number of viral genomes in poliovirus-infected cells in vitro just before the cytopathic effect.…”

Section: Discussionmentioning

confidence: 60%

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Couderc

Christodoulou

Kopecká

et al. 1989

Journal of General Virology

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SUMMARYUsing in situ hybridization techniques for viral RNA and employing a specific riboprobe, we have detected virus in neural cells of monkeys infected with poliovirus type l (PV-1) by the intraspinal route. In monkeys paralysed after inoculation of a neurovirulent revertant of PV-1/Sabin strain, viral RNA was detected in motor neurons and their processes, and in polymorphonuclear and small neural cells. Quantitative in situ hybridization provided evidence of viral replication in individual cells suggesting that the death of motor neurons was due to the direct effect of poliovirus replication in these cells. The histological study of neural lesions of monkeys paralysed after infection with the attenuated Sabin strain of PV-1 revealed two major differences compared to monkeys infected with a virulent strain: (i) the number of destroyed moto r neurons was reduced and limited to the site of inoculation and (ii) the inflammatory reaction was localized but more intense. An account is given of the difference in histopathology induced by virulent and attenuated strains of PV-1 in the central nervous system.

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Section: Discussionmentioning

confidence: 60%

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Couderc

Christodoulou

Kopecká

et al. 1989

Journal of General Virology

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“…Particles were also observed in mature macrophages, both in phagocytic vacuoles and apparently replicating in the cytoplasm. Indications that other picornaviruses replicate in the lamina propria have been noted by Kanamitsu et al (1967) and Heinz and Cliver (1989).…”

Section: G í4 Higher Magnification Of Inclusion (I) In Fig 13 Showmentioning

confidence: 76%

Infectious stunting syndrome of chickens in Great Britain: Intestinal ultrastructural pathology

Frazier

Reece²

1990

Avian Pathology

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SUMMARYThe ultrastructural pathology of the intestine of field and experimental cases of 4-to 6-day-old chickens showing early signs of stunting syndrome was studied. Changes were most frequently observed in the lamina propria, with infiltrations of lymphoid cells, mesenchymal cells and macrophages. Cysts were observed in the crypts. Early, small cysts were lined with both epithelial cells and myofibroblasts, with no underlying basment membrane. Larger cysts were composed of cuboidal epithelial cells surrounded by a basement membrane with underlying fibroblasts and collagen fibrils.Membrane-bound cytoplasmic inclusions containing picornavirus-like particles about 20 nm in diameter were present in mesenchymal cells and macrophages in the lamina propria, both at the base of the villi and in the corium of the villus. Cells containing particles were associated with early cysts, but not with large, mature cysts. Particles were occasionally observed in enterocytes, particularly in field cases.A brief description of the normal chick intestinal lamina propria is also included.

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“…To date, whether epithelial or lymphoid cells are the primary sites of poliovirus replication in the gut has remained a matter of debate (4,9). Previously, fluorescence-labeled immunoglobulin from a poliovirus-infected macaque was used to detect poliovirus in epithelia or speculative macrophages after viral feeding (15). Technical difficulties, including nonspecific stain- Mahoney type 1 poliovirus.…”

Section: Resultsmentioning

confidence: 99%

Pathogenic Events in a Nonhuman Primate Model of Oral Poliovirus Infection Leading to Paralytic Poliomyelitis

Shen

Chen

Huang

et al. 2017

J Virol

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Despite a great deal of prior research, the early pathogenic events in natural oral poliovirus infection remain poorly defined. To establish a model for study, we infected 39 macaques by feeding them single high doses of the virulent Mahoney strain of wild type 1 poliovirus. Doses ranging from 10 7 to 10 9 50% tissue culture infective doses (TCID 50 ) consistently infected all the animals, and many monkeys receiving 10 8 or 10 9 TCID 50 developed paralysis. There was no apparent difference in the susceptibilities of the three macaque species (rhesus, cynomolgus, and bonnet) used. Virus excretion in stool and nasopharynges was consistently observed, with occasional viremia, and virus was isolated from tonsils, gut mucosa, and draining lymph nodes. Viral replication proteins were detected in both epithelial and lymphoid cell populations expressing CD155 in the tonsil and intestine, as well as in spinal cord neurons. Necrosis was observed in these three cell types, and viral replication in the tonsil/gut was associated with histopathologic destruction and inflammation. The sustained response of neutralizing antibody correlated temporally with resolution of viremia and termination of virus shedding in oropharynges and feces. For the first time, this model demonstrates that early in the infectious process, poliovirus replication occurs in both epithelial cells (explaining virus shedding in the gastrointestinal tract) and lymphoid/monocytic cells in tonsils and Peyer's patches (explaining viremia), extending previous studies of poliovirus pathogenesis in humans. Because the model recapitulates human poliovirus infection and poliomyelitis, it can be used to study polio pathogenesis and to assess the efficacy of candidate antiviral drugs and new vaccines.IMPORTANCE Early pathogenic events of poliovirus infection remain largely undefined, and there is a lack of animal models mimicking natural oral human infection leading to paralytic poliomyelitis. All 39 macaques fed with single high doses ranging from 10 7 to 10 9 TCID 50 Mahoney type 1 virus were infected, and many of the monkeys developed paralysis. Virus excretion in stool and nasopharynges was consistently observed, with occasional viremia; tonsil, mesentery lymph nodes, and intestinal mucosa served as major target sites of viral replication. For the first time, this model demonstrates that early in the infectious process, poliovirus replication occurs in both epithelial cells (explaining virus shedding in the gastrointestinal tract)

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Immunofluorescent Study on the Pathogenesis of Oral Infection of Poliovirus in Monkey

Cited by 33 publications

References 15 publications

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Molecular Pathogenesis of Neural Lesions Induced by Poliovirus Type 1

Infectious stunting syndrome of chickens in Great Britain: Intestinal ultrastructural pathology

Pathogenic Events in a Nonhuman Primate Model of Oral Poliovirus Infection Leading to Paralytic Poliomyelitis

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