scholarly journals ADAPTATION OF A LANSING STRAIN OF POLIOMYELITIS VIRUS TO NEWBORN MICE

1951 ◽  
Vol 94 (2) ◽  
pp. 111-121 ◽  
Author(s):  
Jordi Casals ◽  
Peter K. Olitsky ◽  
Ralph O. Anslow
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Incubation Period ◽  
Newborn Mice ◽  
Poliomyelitis Virus ◽  
New Born ◽  
The Central Nervous System ◽  
Almost All ◽  
Experimental Disease

By means of rapid serial passages, including 3 successive "blind" passages, the MEF1 strain, a Lansing-type poliomyelitis virus, has been adapted to new-born mice. The virus can readily be propagated in newborn mice, in which fully adapted virus induces in almost all inoculated animals the experimental disease, resulting in a much greater infectivity for the central nervous system and a uniformly short and regular incubation period.

On the incubation period in neurolues

1927 ◽  
Vol 23 (10) ◽  
pp. 1046-1050
Author(s):  
E. V. Sukhova
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Incubation Period ◽  
The Other ◽  
Other Hand ◽  
General Number ◽  
The Central Nervous System

Speaking about syphilis lesions of the central nervous system, it is impossible not to note that these lesions are among the most severe diseases of the latter. But, on the other hand, their severity is redeemed to some extent by the specific means of combating them which we have in our hands. In this case, the fight against neurolues is reduced not so much to its treatment as to its prevention. Hence the interest with which the question of the influence of various conditions on the occurrence of syphilitic lesions of the central nervous system has recently begun to be comprehensively discussed and the exact causes which, from the general number of syphilitics, distinguish the group subsequently condemned to neurolues have been sought to be elucidated.

scholarly journals Central Nervous System Cell-Derived Exosomes in Neurodegenerative Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yang Tian ◽  
Chen Fu ◽  
Yifan Wu ◽  
Yao Lu ◽  
Xuemei Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Extracellular Vesicles ◽  
Mammalian Cells ◽  
Glia Cells ◽  
Central Nervous System Cell ◽  
The Central Nervous System ◽  
System Cell ◽  
Almost All

Exosomes are a type of extracellular vesicles secreted by almost all kinds of mammalian cells that shuttle “cargo” from one cell to another, indicative of its role in cell-to-cell transportation. Interestingly, exosomes are known to undergo alterations or serve as a pathway in multiple diseases, including neurodegenerative diseases. In the central nervous system (CNS), exosomes originating from neurons or glia cells contribute to or inhibit the progression of CNS-related diseases in special ways. In lieu of this, the current study investigated the effect of CNS cell-derived exosomes on different neurodegenerative diseases.

scholarly journals Reovirus Neurotropism and Virulence Are Dictated by Sequences in the Head Domain of the Viral Attachment Protein

2018 ◽  
Vol 92 (23) ◽  
Author(s):  
Danica M. Sutherland ◽  
Pavithra Aravamudhan ◽  
Melanie H. Dietrich ◽  
Thilo Stehle ◽  
Terence S. Dermody
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ependymal Cells ◽  
Attachment Protein ◽  
Newborn Mice ◽  
Viral Attachment ◽  
Head Domain ◽  
Serotype 1 ◽  
The Central Nervous System ◽  
The Brain

ABSTRACTViral capsid components that bind cellular receptors mediate critical functions in viral tropism and disease pathogenesis. Mammalian orthoreoviruses (reoviruses) spread systemically in newborn mice to cause serotype-specific disease in the central nervous system (CNS). Serotype 1 (T1) reovirus infects ependymal cells to cause nonlethal hydrocephalus, whereas serotype 3 (T3) reovirus infects neurons to cause fulminant and lethal encephalitis. This serotype-dependent difference in tropism and concomitant disease is attributed to the σ1 viral attachment protein, which is composed of head, body, and tail domains. To identify σ1 sequences that contribute to tropism for specific cell types in the CNS, we engineered a panel of viruses expressing chimeric σ1 proteins in which discrete σ1 domains have been reciprocally exchanged. Parental and chimeric σ1 viruses were compared for replication, tropism, and disease induction following intracranial inoculation of newborn mice. Viruses expressing T1 σ1 head sequences infect the ependyma, produce relatively lower titers in the brain, and do not cause significant disease. In contrast, viruses expressing T3 σ1 head sequences efficiently infect neurons, replicate to relatively higher titers in the brain, and cause a lethal encephalitis. Additionally, T3 σ1 head-expressing viruses display enhanced infectivity of cultured primary cortical neurons compared with T1 σ1 head-expressing viruses. These results indicate that T3 σ1 head domain sequences promote infection of neurons, likely by interaction with a neuron-specific receptor, and dictate tropism in the CNS and induction of encephalitis.IMPORTANCEViral encephalitis is a serious and often life-threatening inflammation of the brain. Mammalian orthoreoviruses are promising oncolytic therapeutics for humans but establish virulent, serotype-dependent disease in the central nervous system (CNS) of many young mammals. Serotype 1 reoviruses infect ependymal cells and produce hydrocephalus, whereas serotype 3 reoviruses infect neurons and cause encephalitis. Reovirus neurotropism is hypothesized to be dictated by the filamentous σ1 viral attachment protein. However, it is not apparent how this protein mediates disease. We discovered that sequences forming the most virion-distal domain of T1 and T3 σ1 coordinate infection of either ependyma or neurons, respectively, leading to mutually exclusive patterns of tropism and disease in the CNS. These studies contribute new knowledge about how reoviruses target cells for infection in the brain and inform the rational design of improved oncolytic therapies to mitigate difficult-to-treat tumors of the CNS.

KINKY HAIR DISEASE

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 181-183
Author(s):  
John H. Menkes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
In Utero ◽  
Degenerative Disease ◽  
Degenerative Diseases ◽  
Kinky Hair Disease ◽  
The Central Nervous System ◽  
Almost All ◽  
Enzymatic Defect ◽  
Kinky Hair

Despite many recent advances in our understanding of progressive degenerative diseases of the nervous system which have permitted us in some instances to define the underlying enzymatic defect and to detect the disease in utero, treatment for affected children has been nonexistent in almost all instances. The paper by Danks et al.1 in this issue of Pediatrics is, therefore, of considerable importance. It not only demonstrates the underlying cause for one of these disorders, Kinky Hair disease, but also suggests a relatively simple course of treatment. Ten years ago a group of Residents from the Departments of Neurology, Pediatric Neurology, Neuropathology, and Dermatology described in this journal2 what appeared to be a new degenerative disease of the central nervous system.

scholarly journals Distribution of Serotonergic Neurons in the Central Nervous System: A Peroxidase-Antiperoxidase Study with Anti-Serotonin Antibodies

1983 ◽  
Vol 31 (1A_suppl) ◽  
pp. 181-185 ◽  
Author(s):  
Y. Takeuchi ◽  
H. Kimura ◽  
T. Matsuura ◽  
T. Yonezawa ◽  
Y. Sano
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuronal Somata ◽  
Immunohistochemical Technique ◽  
Interspecific Differences ◽  
System A ◽  
Highly Sensitive ◽  
Serotonin Antibodies ◽  
The Central Nervous System ◽  
Almost All

Distribution of serotonin (5-HT) neurons in the central nervous system (CNS) of various vertebrates was investigated with a highly sensitive immunohistochemical technique. Antibodies were raised in rabbits against an antigen prepared by coupling 5-HT to bovine thyroglobulin. 5-HT neurons were found to be distributed more widely and densely than has been heretofore described. Serotonergic neuronal somata are organized according to certain basic patterns, but there are interspecific differences with regard to the distribution of 5-HT fibers. The processes of 5-HT neurons form a dense plexus by ramification and anastomosis in almost all areas of the CNS, including the ventricular surfaces. In the light of our observations, Golgi's reticular theory may have to be revised.

scholarly journals EXPERIMENTAL STUDIES OF THE VIRUS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

1939 ◽  
Vol 70 (6) ◽  
pp. 565-582 ◽  
Author(s):  
Peter K. Olitsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Experimental Studies ◽  
Vitreous Body ◽  
Host Susceptibility ◽  
Laboratory Animals ◽  
Blood Sucking ◽  
The Central Nervous System ◽  
Experimental Disease ◽  
Infective Agent

The results of investigations thus far carried out on experimental avian encephalomyelitis indicate that the virus of this newly described disease conforms to the group of definitely established viruses. It was essential to determine its taxonomy since the only prior record of its study (1) defines the infective agent as a virus because the usual cultural attempts failed to reveal a visible microorganism to be identified with it, and because the transmissible agent passed through Seitz and Berkefeld N filters. At the present time such determinants fail completely to satisfy the criteria for defining a virus and their acceptance would lead to the inclusion of certain filtrable microbic agents, difficult to reveal except by special cultural procedures, as viruses (10). The virus of avian encephalomyelitis is distinct from that of equine encephalomyelitis and is clearly a virus sui generis. The striking feature of its properties is its narrow range of host susceptibility—only the avian species are responsive to inoculation; ordinary laboratory animals are apparently resistant, even to large numbers of chicken cerebral infective doses. In addition, it is probable that its size is in the range of that of the equine virus. Studies also reveal that the virus is not easily sedimented by centrifugation (that is, at 5400 R.P.M. for one hour in the angle centrifuge and at 12,000 R.P.M. for one hour in the open air centrifuge) and is resistant to the action of glycerol and to drying. It is readily filtrable through Seitz one and two disc filters, through Berkefeld V and N candles, and is active in dilutions in broth up to 10–6. It passes through gradocol membranes of 73 mµ average pore diameter at least (the end-point has not as yet been definitely determined). An attack of the experimental disease leads to development of resistance to reinoculation and of antibodies in the serum. Old birds are reported as being refractory to infection, both in nature and in the laboratory (1, 2). Whether this resistance in mature animals is due to earlier exposure to infection, or to the development of structural or physiological barriers to invasion by the virus, remains still to be determined. Under experimental conditions, the route by which the virus acts uniformly to induce disease is the intracerebral. Yet in certain instances other peripheral ways of inoculation such as the intraperitoneal, subcutaneous, intradermal, intravenous, intramuscular, intrasciatic, may also be effective. Thus far, in limited experiments, feeding, or instilling nasally, or injecting into the vitreous body the infective agent has been ineffective. Whether the viral progression is axonal from peripheral sites is still to be determined; as should be also the question whether it multiplies in any of the organs other than the central nervous tissues. The virus was not detected in the blood during the period of incubation or during the acute phases of the experimental disease. So that unless it is found that other animals harbor the virus, or that still other sources of it exist as yet not disclosed, it is not likely that the disease is disseminated by a blood-sucking insect. The actual portal of entry and the factor in the spread of the disease in nature is still obscure, since the evidence here presented is still too incomplete to elucidate these problems. The pathological lesions induced are of interest. The neuronal reaction resembles that brought about by axonal disturbance (axon reaction, Nissl's or retrograde degeneration). The question may well be asked whether there may not be here an initial injury by the virus to the axonal process of the neuron, which in turn induces the retrograde changes in the cell body. This has as yet to be studied, as well as the possibility of viral progression along an axonal route with or without concurrent multiplication. The significance of the second major lesion in the central nervous system, namely, the generally marked perivascular reaction, is also still to be determined. Finally, the only observable and histopathological change in organs other than the central nervous tissues (in which we have not as yet noted the change) is in the hyperplasia of the normally present lymphoid islands. One is impressed by the prodigious numbers of lymphoid elements surrounding the vessels of the central nervous system and the question here is whether these hyperplastic areas serve as depots to supply the cells for this perivascular reaction.

THE CENTRAL NERVOUS SYSTEM IN THE NEW-BORN

1966 ◽  
Vol 22 (1) ◽  
pp. 49-55 ◽  
Author(s):  
R. J. ROBINSON ◽  
J. P. M. TIZARD
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
New Born ◽  
The Central Nervous System

scholarly journals THE PROTECTIVE ACTION OF TRYPAN RED AGAINST INFECTION BY A NEUROTROPIC VIRUS

1945 ◽  
Vol 82 (5) ◽  
pp. 297-309 ◽  
Author(s):  
Harland G. Wood ◽  
Irving I. Rusoff
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Congo Red ◽  
Protective Action ◽  
High Concentration ◽  
Critical Test ◽  
Poliomyelitis Virus ◽  
Cotton Rats ◽  
The Central Nervous System ◽  
The Difference

Trypan red, when injected intraperitoneally into mice, has been found greatly to lower the incidence of the infection of mice inoculated intraperitoneally with the neurotropic MM virus. The protective action of the dye is overcome if the virus is inoculated in too high concentration. The lowered incidence of infection was observed in mice inoculated with virus for as long as 29 days after the last dye injection. Of a number of dyes tested, trypan red, brilliant vital red, and Congo red were found effective. In cotton rats inoculated intraperitoneally with MM virus, trypan red was likewise found to lower the incidence of infection. With monkeys and a typical poliomyelitis virus no protection was observed against the virus inoculated intraperitoneally. The latter experiment is considered to have been inadequate for a critical test of the effect of trypan red on poliomyelitis infection. When either the MM virus or Lansing virus were inoculated intracerebrally into mice, the effect of the dye on incidence of infection was small. In the case of the Lansing virus the difference was statistically significant, however. The possible relation of alteration in the permeability of the barrier between the blood and the central nervous system as a cause of the effect of trypan red is discussed.

scholarly journals Postmortem Quantitative Analysis of Prion Seeding Activity in the Digestive System

Molecules ◽  
2019 ◽  
Vol 24 (24) ◽  
pp. 4601 ◽  
Author(s):  
Katsuya Satoh ◽  
Takayuki Fuse ◽  
Toshiaki Nonaka ◽  
Trong Dong ◽  
Masaki Takao ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Quantitative Analysis ◽  
Prion Protein ◽  
Neurodegenerative Disorders ◽  
Digestive System ◽  
Prion Diseases ◽  
Jakob Disease ◽  
The Central Nervous System ◽  
Almost All

Human prion diseases are neurodegenerative disorders caused by prion protein. Although infectivity was historically detected only in the central nervous system and lymphoreticular tissues of patients with sporadic Creutzfeldt-Jakob disease, recent reports suggest that the seeding activity of Creutzfeldt-Jakob disease prions accumulates in various non-neuronal organs including the liver, kidney, and skin. Therefore, we reanalyzed autopsy samples collected from patients with sporadic and genetic human prion diseases and found that seeding activity exists in almost all digestive organs. Unexpectedly, activity in the esophagus reached a level of prion seeding activity close to that in the central nervous system in some CJD patients, indicating that the safety of endoscopic examinations should be reconsidered.

scholarly journals THE INTRACELLULAR DISTRIBUTION OF LANSING POLIOMYELITIS VIRUS IN THE CENTRAL NERVOUS SYSTEM OF INFECTED COTTON RATS

1952 ◽  
Vol 96 (2) ◽  
pp. 121-136 ◽  
Author(s):  
Carlton E. Schwerdt ◽  
Arthur B. Pardee
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracellular Distribution ◽  
Particle Fraction ◽  
Poliomyelitis Virus ◽  
Cotton Rats ◽  
The Central Nervous System

A procedure has been described for the centrifugal fractionation of the cellular particulate components of CNS tissue infected with poliomyelitis virus. A study of the distribution of infectivity among these components revealed that approximately four-fifths of the virus is found free in the submicroscopic particle fraction. The validity of the conclusion that the virus is located in this fraction of the intact neuron is discussed.

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