Experimental Parainfluenza Type 1 Virus-Induced Encephalopathy in Adult Mice

Zgórniak-Nowosielska, I; Iwasaki, Yuzo; Tachovsky, Thomas G.; Tanaka, Ryuichi; Koprowski, Hilary

doi:10.1001/archneur.1976.00500010057009

Cited by 12 publications

(5 citation statements)

References 14 publications

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“…Since the report on isolation of an agent resembling type 1 parainfluenza virus from the brain tissue of a patient with multiple sclerosis (21), the pathogenicity of parainfluenza virus in CNS has attracted the attention, and many investigations about neurovirulence of the agent have been reported (5,6,11,14,22).…”

Section: Discussionmentioning

confidence: 99%

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Shimokata

1978

Microbiology and Immunology

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The pathogenicity of parainfluenza type 2 (croup-associated) virus known to cause infections of the respiratory tract in the early life of man was studied in the brain of mice. One-to 4-day-old sucklings and 4-week-old mice were inoculated intracerebrally with the virus. The virus multiplied in sucklings, but not in adults. Most mice inoculated intracerebrally with the virus appeared healthy. Histological examination showed minimum inflammatory changes, although moderate hydrocephalus developed in three of twenty-one sucklings by 6 weeks post-infection. Immunofluorescent study in sucklings showed viral antigens in ependymal lining cells and choroid plexus epithelium during the first two weeks, and parenchymal cells for more than two months. Virus specific antibody response was observed in adults, but not in sucklings. One interesting finding was that viral antigens persisted in six out of 11 suckling brains for one to two months.

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Section: Discussionmentioning

confidence: 99%

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Shimokata

1978

Microbiology and Immunology

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“…Since these original epidemiological studies, much work has focused on identification of pathogens that may trigger disease. The most commonly implicated class of pathogens in the development of MS is viruses (86)(87)(88)(89)(90)(91)(92)(93)(94).…”

Section: Multiple Sclerosis -A Short Coursementioning

confidence: 99%

Impact of Erb-B Signaling on Myelin Repair in the CNS Following Virus-Induced Damage

Drescher¹

2009

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS.

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Section: Multiple Sclerosis -A Short Coursementioning

confidence: 99%

“…Viruses have been implicated or eliminated as causes of the disease based on their presence or absence in a demyelinating lesion, or the level of virus-specific antibody in the patient at or near diagnosis. Some of the pathogens proposed as triggers of MS include rabies (86,87), human herpes virus 6 (95, 96), measles (96-100), adenovirus (88)(89), parainfluenza type 1 (90)(91)(92)(93)101), rhinovirus (102), and Epstein Barr virus (94, 103, 104).…”

Section: Multiple Sclerosis -A Short Coursementioning

confidence: 99%

Being a mouse in a man's world: what TMEV has taught us about human disease

Drescher

Sоsnowska

2008

Front Biosci

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Choosing an appropriate animal model to study a disease is guided by a variety of factors including but not limited to the questions being asked, availability of reagents, knowledge of the animal species, personal biases of the researcher, and in some cases, cost and availability of facilities to effectively investigate the model. The validity of an animal model can be further complicated when the etiology of the disease is incompletely defined. Examples of these diseases include multiple sclerosis (MS) and type 1 diabetes (T1D). In addition to host genetics, epidemiological studies have implicated infectious agents, in particular viruses as triggers of these diseases. Thus many studies of these diseases have focused on modeling the interactions of viruses and the host immune response in vivo in small animals. Theiler's murine encephalomyelitis virus (TMEV) infection of mice has been used for over 30 years as a model of virus-induced demyelination. TMEV induces a MS-like disease in susceptible strains of mice but does not cause pathology in humans. While some researchers may question the rationale for using a non-human pathogen to model human disease, the TMEV model of central nervous system (CNS) demyelination has permitted study of some aspects of human MS which would have been difficult to address in other models of the disease. Despite being 'merely a disease of mice,' many of the findings in the Theiler's virus model are directly applicable to the human condition, and studies from the model are responsible for our current understanding of mechanisms of pathology and clinical disability in human MS. In this review we will present some of the key findings from the TMEV model in the context of human disease.

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Experimental Parainfluenza Type 1 Virus-Induced Encephalopathy in Adult Mice

Cited by 12 publications

References 14 publications

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Studies on the Pathogenicity of Human‐Origin Parainfluenza Virus in the Brain of Mice

Impact of Erb-B Signaling on Myelin Repair in the CNS Following Virus-Induced Damage

Being a mouse in a man's world: what TMEV has taught us about human disease

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