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.

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 Intracellular distribution of pentobarbital sodium in rat brain

1958 ◽  
Author(s):  
◽  
Carol Jean Oen
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Rat Brain ◽  
Major Effect ◽  
Cellular Component ◽  
Intracellular Distribution ◽  
Brain Cells ◽  
Pentobarbital Sodium ◽  
The Central Nervous System ◽  
The Way

"The major effect of the barbiturates is depression of the central nervous system, but the way in which these drugs exert their effect is not yet well understood...As the biochemical functions of the cell and its various parts become better understood, it is of interest to relate the actions of t a drug to some particular function (Reiner and Gellhorn, 1956). If it were found that barbiturate were localized by a particular cellular component, this might mean that its effect was rendered through some function of that particular component. Consequently, this study was undertaken to determine the intracellular distribution of a particular barbiturate, pentobarbital sodium, within rat brain cells."--Introduction

scholarly journals THE EFFECT OF CATAPHORESIS ON POLIOMYELITIS VIRUS

1929 ◽  
Vol 50 (3) ◽  
pp. 273-277 ◽  
Author(s):  
P. K. Olitsky ◽  
C. P. Rhoads ◽  
P. H. Long
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune Serum ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Active Stage ◽  
Electrical Field ◽  
Hydrogen Ion Concentration ◽  
Poliomyelitis Virus ◽  
The Central Nervous System

1. Under ordinary conditions of hydrogen ion concentration the virus of poliomyelitis, as such, or associated with particles in fine suspension, migrates in an electrical field to the anode. It follows that the virus bears an electronegative charge. 2. By means of cataphoresis, the virus can be recovered from a non-infective mixture of virus and specific immune serum. 3. By the same means it is possible to reveal the presence of virus in the central nervous system of a monkey which has recovered from the active stage of experimental poliomyelitis.

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.

scholarly journals STUDIES IN RODENT POLIOMYELITIS

1942 ◽  
Vol 76 (1) ◽  
pp. 31-51 ◽  
Author(s):  
Claus W. Jungeblut ◽  
Rose R. Feiner ◽  
Murray Sanders
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Flaccid Paralysis ◽  
Nerve Tissue ◽  
Subcutaneous Route ◽  
Poliomyelitis Virus ◽  
The Central Nervous System

1. Murine SK poliomyelitis virus has been transferred from mouse to guinea pig with the establishment of a fixed strain of cavian passage virus. 2. The disease thus produced in guinea pigs is characterized by the occurrence of flaccid paralysis. Typical poliomyelitic lesions are found in the anterior horn of the spinal cord. 3. Guinea pigs are susceptible to infection with murine virus by the intracerebral, intravenous, intraperitoneal, and subcutaneous route; cavian passage virus produces paralysis only upon intracerebral or intravenous injection. Neither virus paralyzes guinea pigs by feeding or nasal instillation. 4. The potency of the virus (murine or cavian) in guinea pigs is considerably lower than in mice and compares with the titer of the original SK strain in monkeys. In paralyzed guinea pigs the virus is found only in the central nervous system and not in extraneural sites, such as blood or abdominal viscera. 5. Attempts to cultivate cavian passage virus in tissue culture have yielded evidence of some in vitro propagation but no passage virus has as yet been obtained by this method. 6. Cross neutralization tests with cavian passage virus in guinea pigs and with murine virus in mice have established the serological identity of the two viruses. Inactivation of cavian passage virus in guinea pigs by poliomyelitis-convalescent monkey sera is irregular. Complete neutralization has been obtained with a concentrated poliomyelitis horse serum. 7. Resistance to reinfection with potent virus can be demonstrated in convalescent guinea pigs as well as in guinea pigs which have survived a symptomless infection with either murine or cavian virus. This immunity is demonstrable by the power of the serum of such animals to neutralize the virus in vitro and by the ability of nerve tissue to dispose in vivo of the infectious agent. 8. Cavian passage virus has a limited pathogenicity for rhesus monkeys. Of a total of 35 monkeys injected intracerebrally with guinea pig passage virus 26 failed to respond with any manifest symptoms of disease; 8 monkeys showed various signs of definite involvement of the central nervous system consisting of tremor, convulsions, facial palsy, and localized pareses; 1 monkey developed typical flaccid paralysis. 9. Following injection with cavian virus the virus may be recovered from the tissues of normal monkeys but not from the tissues of convalescent monkeys shortly after a paralyzing attack of poliomyelitis due to SK or Aycock virus. 10. Immunization of monkeys with early cavian passage virus by the subcutaneous route has given no clear-cut evidence of protection against intracerebral reinfection with SK poliomyelitis virus. Neither has there been any evidence of effective interference in monkeys injected intravenously with early cavian passage virus and intracerebrally with RMV poliomyelitis virus. 11. The bearing of the experimental data upon the epidemiology of the human disease is discussed.

scholarly journals MULTIPLICATION AND SPREAD OF THE VIRUS OF ST. LOUIS ENCEPHALITIS IN MICE WITH SPECIAL EMPHASIS ON ITS FATE IN THE ALIMENTARY TRACT

1947 ◽  
Vol 85 (6) ◽  
pp. 647-662 ◽  
Author(s):  
John L. Peck ◽  
Albert B. Sabin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intestinal Tract ◽  
Antiviral Agent ◽  
Nerve Fibers ◽  
Human Beings ◽  
Poliomyelitis Virus ◽  
Virus Content ◽  
The Central Nervous System ◽  
The Brain

1. Beginning at 24 hours after intravenous injection of about 10 million intracerebral LD50 of virus there was evidence of simultaneous, progressive multiplication in the brain and intestinal tract. 2. When the virus was introduced directly into the brain or the nasal cavities and mouth, none was found in the intestinal tract until there was general centrifugal spread from the central nervous system during the last stages of the infection at 96 or 120 hours after inoculation when the virus in the entire brain had reached a concentration of about 3 billion LD50. 3. Centrifugal spread began when the virus in the brain reached a concentration of about 400 million LD50 and virus appeared in the pharynx, tongue, and adrenals before it was demonstrable in the intestinal tract, blood, or viscera such as the spleen, liver, and kidneys. 4. Despite the high concentrations of virus which developed in the intestinal tract following intravenous inoculation, it was not demonstrable in the stools, differing in this respect from Theiler's virus in mice and poliomyelitis virus in human beings and monkeys. 5. No antiviral agent was found in the stools, but the urine of normal mice having a pH of 5.6, inactivated large amounts of St. Louis encephalitis virus. 6. There was no evidence of multiplication in the nasal mucosa of mice which succumbed with encephalitis following nasal instillation of the virus, the course of events being comparable in this respect to the behavior of the M.V. poliomyelitis virus in rhesus monkeys. 7. At the terminal stage of infection the virus content per milligram of tissue was as great in the leg muscles as in the sciatic nerves. Since this was also true for the urinary bladder, heart, lungs, and tongue among other tissues, and since the amount in the blood was too negligible to account for it, it would appear that the virus either accumulated in these tissues by diffusion from the nerve fibers, along which it was spreading from the central nervous system, or that it multiplied in some constituent other than the nerve fibers.

scholarly journals THE GROWTH CURVE OF THE LANSING STRAIN OF POLIOMYELITIS VIRUS IN THE CENTRAL NERVOUS SYSTEM OF THE MOUSE

1952 ◽  
Vol 95 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John D. Ainslie
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Growth Curve ◽  
Clinical Signs ◽  
Virus Suspension ◽  
Poliomyelitis Virus ◽  
The Central Nervous System ◽  
Infectivity Titer ◽  
The Brain

After intracerebral inoculation of mice with a 10 per cent suspension (approximately 2000 LD50) of the Lansing strain of poliomyelitis virus, the infectivity titer in the brain decreased for approximately 6 hours. It then rose rapidly for 12 to 18 hours to reach titers of over 10–4. The rise in titer in the spinal cord closely paralleled that in the brain for 18 hours, after which the titer surpassed that in the brain by as much as one log. The infectivity titers in the central nervous system of unparalyzed mice remained between 10–3.5 and 10–4.2 for at least 7 days. With the onset of paralysis it was found that the titer was consistently and significantly higher in the spinal cords of paralyzed mice than in their brains or in the brains or cords of unparalyzed mice. After inoculation of 1 per cent virus suspension the increase in titer occurred about 9 hours later than after the inoculation of 10 per cent virus suspension, and the onset of clinical signs of illness was also delayed. Once the titers began to rise, the rate was the same after the inoculation of either concentration of virus, and the maximal levels reached were the same. With both concentrations of virus, maximal infectivity titers in non-paralyzed mice were reached about 9 hours before the onset of signs of poliomyelitis. The significance of these findings is discussed.

scholarly journals FATE OF NASALLY INSTILLED POLIOMYELITIS VIRUS IN NORMAL AND CONVALESCENT MONKEYS WITH SPECIAL REFERENCE TO THE PROBLEM OF HOST TO HOST TRANSMISSION

1938 ◽  
Vol 68 (1) ◽  
pp. 39-62 ◽  
Author(s):  
Albert B. Sabin ◽  
Peter K. Olitsky
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nasal Mucosa ◽  
Rhesus Monkeys ◽  
Olfactory Bulbs ◽  
Poliomyelitis Virus ◽  
The Central Nervous System ◽  
First Time ◽  
The Brain ◽  
Intranasal Instillation

With a method of intranasal instillation of poliomyelitis virus that brings about infection of all M. rhesus monkeys subjected to it, a study was undertaken of the fate of nasally instilled virus in normal and convalescent, immune animals. Control experiments revealed that nasal mucosa of normal monkeys contained no observable antiviral factors and that when five or ten minimal cerebral infective doses were added to the mucosa, virus could be detected by the employed procedure. In the olfactory bulbs even a single infective dose could be recovered, since suspensions of both bulbs could be transferred to the brain of a monkey without any loss of material. After nasal instillation of virus in normal monkeys, it disappeared quickly (4 hours or less) and could be recovered neither from the excised nasal mucosa nor from the olfactory bulbs during the first 48 hours. At 72 hours, just before or coincident with the first rise of temperature, virus was found in very small amounts in the nasal mucosa and for the first time also in the olfactory bulbs. At 96 hours, at least 3 days before the appearance of nervous signs, and later, while virus continued to be present in considerable amounts in the olfactory bulbs (and presumably elsewhere in the central nervous system), none was detected in the nasal mucosa. In convalescent, immune animals receiving the same strain of virus intranasally which caused the original infection, none could be recovered from the nasal mucosa or central nervous system at 4 hours, 1, 2, 3, 4, 5, and 7 days. The bearing of these observations on the problem of host to host transmission of poliomyelitis virus is discussed.

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