scholarly journals CONTRIBUTIONS TO THE PATHOLOGY OF EXPERIMENTAL VIRUS ENCEPHALITIS

1925 ◽  
Vol 41 (3) ◽  
pp. 357-377 ◽  
Author(s):  
Simon Flexner ◽  
Harold L. Amoss
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Herpes Virus ◽  
Neurotropic Activity ◽  
Epidemic Encephalitis ◽  
Virus Encephalitis ◽  
The Central Nervous System ◽  
Herpès Virus ◽  
Experimental Virus

Mild strains of the virus of herpes are described the action of which tends to be confined and local. Unless, therefore, these mild strains are injected intracranially they do not tend to produce virus encephalitis in the rabbit. Recovery from infection with the mild strains confers immunity to virulent strains of the herpes and allied viruses. Long glycerolation reduces the number of viable organisms. This loss among the mild strains may reduce the virus below the strength required for an effective extracranial although not below the strength needed for an intracranial inoculation. Herpes virus carriage in man, even under highly favorable conditions, is difficult of detection by means of rabbit inoculation. The detection may be achieved by intracranial when it cannot be accomplished by intracorneal inoculation. The virus producing encephalitis in the rabbit attaches itself chiefly to and multiplies in the substance of the central nervous system. Hence its detection in the cerebrospinal fluid is rarely accomplished. When the inoculation of the virus is made intracranially and especially when the inoculum is composed of active brain tissue, the virus is discoverable in the cerebrospinal fluid by rabbit inoculation much more frequently than when the virus encephalitis follows an extracranial variety of infection. The herpes virus is capable of excretion by the kidney of the rabbit and of being detected in the urine by rabbit inoculation. Among the rarer symptoms of virus encephalitis is excessive lacrimation. While salivation is frequent, lacrimation is exceptional. A comparison of the Levaditi, Doerr, and Goodpasture strains of virus indicates the first to be of medium, the second of mild, and the third of high degree of neurotropic activity. The Doerr strain resembles the mild herpes strains described in this paper. The Goodpasture virus, while exceeding the Levaditi strain in affinity for the central nervous system, falls below the H. F. strain in this regard. Neutralization of virus by the serum of infected and recovered rabbits takes place regularly within certain quantitative limits. Neutralization with human serum is inconstant and capricious and without demonstrable relation to previous attacks of epidemic encephalitis. Comparison of the clinical types of encephalitis as presented by the epidemic variety in man and the experimental virus variety in rabbits brings out certain correspondences and certain differences. It is only in partial and essentially superficial aspects that the two diseases can be identified one with the other.

scholarly journals CONTRIBUTIONS TO THE PATHOLOGY OF EXPERIMENTAL VIRUS ENCEPHALITIS

1925 ◽  
Vol 41 (2) ◽  
pp. 215-231 ◽  
Author(s):  
Simon Flexner ◽  
Harold L. Amoss
Keyword(s):  
Cerebrospinal Fluid ◽  
Herpes Virus ◽  
Virus Disease ◽  
Brain Structures ◽  
Epidemic Encephalitis ◽  
Virus Encephalitis ◽  
Human Pathology ◽  
B Virus ◽  
Herpès Virus ◽  
The Brain

In this paper is given an account of an inoculable virus disease produced in the rabbit with cerebrospinal fluid taken from a case of vascular and neural syphilis. The study which yielded the results presented was undertaken in the course of an investigation into the etiology of epidemic or lethargic encephalitis. Twenty-seven samples of cerebrospinal fluid, derived from cases of epidemic encephalitis, were tested by us upon rabbits without positive result. The one successful instance in which an inoculable disease was produced arose from the injection of one of three specimens of the cerebrospinal fluid taken from the case of syphilis. Following this success, two subsequent injections of the fluid, taken from the same patient, were made unsuccessfully. Although certain American and European investigators have reported securing a virus from the cerebrospinal fluid of cases of epidemic encephalitis, we have consistently failed in our endeavors to confirm their results. However, we believe that the finding of the J. B. virus may serve to clarify the obscurity and confusion now enveloping the so called virus of encephalitis. It had previously been shown that no biological differences could be detected between the herpes and the encephalitis strains of virus. The former, as is well known, is readily secured by inoculating rabbits with the contents of herpes vesicles, while the latter has, at best, been obtained with great difficulty. The J. B. virus agrees biologically with the herpes and encephalitis strains of virus. It is our opinion that the J. B. virus is merely a herpes virus which has gained access to the cerebrospinal fluid and, at the time of inoculation of the rabbits, was present in a concentration sufficing to induce virus encephalitis. The fact, if fact it is proved to be, that the herpes virus may find its way into the cerebrospinal fluid opens to question all the supposed instances of successful implantation of a virus of epidemic encephalitis upon the rabbit. It is indeed highly probable that, in so far as such a virus has been found at all in the cerebrospinal fluid, it also is a specimen of the herpes virus. Our studies lead us to suppose that at best it is an infrequent event for the herpes virus to occur in demonstrable form in the cerebrospinal fluid. Perhaps a more delicate means of detection than the rabbit inoculation would serve to reveal the presence oftener. It is known that strains of herpes virus of greater or less intensity of action for rabbits exist. It is, of course, possible that we discover, by present methods, only the highly active strains and those only when chancing to be present in a certain concentration. We inoculated 100 specimens of cerebrospinal fluid and obtained in a single instance the virus infection of the rabbit. In all respects the J. B. virus agrees in intensity of effect, in mode of attack upon the cornea, skin, and brain, and in immunization responses, with the true strains of herpes virus and the so called strains of encephalitis virus. If, as the above statements indicate, all the virus strains of the class considered are examples of the herpes virus, it follows that the etiology of epidemic encephalitis remains entirely unresolved. It is highly improbable that the ubiquitous herpes virus plays the kind of part in human pathology which it has been shown to play in experimental rabbit pathology. While the active strains of that virus possess a strong affinity for the brain structures of the rabbit, the virus has not in the past shown any selective affinity for the brain of man. To ascribe epidemic encephalitis in man to particular and peculiar varieties of the herpes virus is, with our present knowledge, unwarranted.20 The wide variations in histological lesions described in the brain of rabbits succumbing to herpes or virus encephalitis raise the question of the essential manner of action of the virus upon the brain tissues. Hitherto it has been the cellular infiltrative lesions which have been emphasized. We have, however, learned that very extensive infiltrations about blood vessels and in the brain substance may exist independently of even mild symptoms of disease.16 The question is propounded, therefore, whether the herpes virus does not attack nerve cells directly, affecting them quantitatively in such ways as at one time to produce stimulation and at another time paralysis. The manifold symptoms of virus encephalitis in the rabbit are open to this interpretation. In order, however, to base this notion on microscopical findings, a more subtle technique than hitherto widely employed is required. A histological restudy of the subject is being made with this view in mind. The name virus encephalitis is proposed for the experimental disease produced in rabbits by the inoculation of the herpes and allied viruses.

scholarly journals CONTRIBUTIONS TO THE PATHOLOGY OF EXPERIMENTAL VIRUS ENCEPHALITIS

1928 ◽  
Vol 47 (1) ◽  
pp. 23-36 ◽  
Author(s):  
Simon Flexner
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Herpes Virus ◽  
Epidemic Encephalitis ◽  
Virus Encephalitis ◽  
Active Virus ◽  
Brain Involvement ◽  
Herpès Virus ◽  
Experimental Virus ◽  
The Brain

The guinea pig is subject to cerebral and corneal inoculation of the herpes virus. The effects of the inoculations vary with the strength or degree of virulence of the virus. Weak strains of the virus are implanted on the cerebrum with difficulty and strong strains with ease. Weak strains are quickly suppressed by the brain and strong strains may be passed indefinitely from brain to brain of the guinea pig. Strains of intermediate potency can be passed for a limited number of times only. Weak strains induce keratoconjunctivitis without brain involvement, while strong strains invade the brain from the eye and produce fatal encephalitis. In the latter case, the brain contains active virus inoculable upon the cornea and into the brain of rabbits and guinea pigs. Strains of intermediate potency produce keratoconjunctivitis accompanied by mild symptoms of encephalitis, from which recovery results. The guinea pig serves even more definitely than the rabbit to distinguish grades of virus according to strength or virulence. There is no difference of kind but only of degree of response to inoculation of herpes virus in the rabbit and the guinea pig. The etiology of epidemic encephalitis has not, therefore, been brought appreciably nearer solution by experiments with herpes virus carried out in guinea pigs.

HERPES VIRUS-LIKE DNA SEQUENCES IN PRIMARY NON HODGKIN LYMPHOMAS OF THE CENTRAL NERVOUS SYSTEM

1996 ◽  
Vol 55 (5) ◽  
pp. 623 ◽  
Author(s):  
Jacqueline Mikol ◽  
Martine Deplanche ◽  
Antoine Moullnier ◽  
Bertrand Dupont ◽  
Frédéric Morinet
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Dna Sequences ◽  
Herpes Virus ◽  
The Central Nervous System ◽  
Herpès Virus

CHAPTER 9: Immunology of TBEV-Infections

2020 ◽  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Nk Cells ◽  
Peripheral Blood ◽  
Sample Collection ◽  
Tick Borne Encephalitis ◽  
Viral Infectious Disease ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.

scholarly journals Development of the Cerebrospinal Fluid in Early Stage after Hemorrhage in the Central Nervous System

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Petr Kelbich ◽  
Aleš Hejčl ◽  
Jan Krejsek ◽  
Tomáš Radovnický ◽  
Inka Matuchová ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Early Stage ◽  
Rank Test ◽  
Signed Rank ◽  
Signed Rank Test ◽  
The Central Nervous System ◽  
Poor Outcomes ◽  
Molecular Patterns

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.

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