scholarly journals EFFECT OF REPEATED FREEZING (–185°C.) AND THAWING ON COLON BACILLI, VIRUS III, VACCINE VIRUS, HERPES VIRUS, BACTERIOPHAGE, COMPLEMENT, AND TRYPSIN

1927 ◽  
Vol 45 (1) ◽  
pp. 11-21 ◽  
Author(s):  
T. M. Rivers
Keyword(s):  
Herpes Virus ◽  
Active Agent ◽  
Vaccine Virus ◽  
Repeated Freezing ◽  
Herpès Virus

Colon bacilli, Virus III, vaccine virus, herpes virus, bacteriophage, complement, and trypsin are either killed or inactivated by repeated freezing (–185°C.) and thawing. As might be expected, some of the agents are more resistant than others. Hence it may be concluded that destruction or inactivation of an active agent by repeated freezing (–185°C.) and thawing is not proof that it was possessed of life.

scholarly journals THE ACTION OF THE LEVADITI STRAIN OF HERPES VIRUS, AND OF VACCINE VIRUS IN THE GUINEA PIG

1928 ◽  
Vol 48 (3) ◽  
pp. 379-391 ◽  
Author(s):  
Peter K. Olitsky ◽  
Perrin H. Long
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Herpes Virus ◽  
Vaccine Virus ◽  
Experimental Conditions ◽  
Two Samples ◽  
Vesicular Stomatitis ◽  
Cross Immunity ◽  
Herpès Virus ◽  
The Brain

A number of methods have been employed in attempts to induce encephalitis in guinea pigs with the Levaditi C strain of herpes virus. Some of these consisted of different modes of inoculation of the virus itself and others of different ways of combining it with vesicular stomatitis and neurovaccine viruses so as to obtain the concomitant effects of both. In still another test the Levaditi virus was combined with the neurovaccine in a manner calculated to bring about the maximum action of each at the same time. By all these methods, the Levaditi virus failed to evoke the characteristic encephalitis which this specimen is capable of inducing uniformly in rabbits. On the other hand, when the Levaditi herpes virus is inoculated into the brain of guinea pigs in conjunction with suitably timed corneal injections, it acquires active encephalitogenic properties. The results just noted suggest several considerations: 1. The possibility of increasing the virulence of a filtrable virus by animal passage in a special manner. It is not likely that the increase as observed was due to dosage, for after the virus acquired its encephalitogenic property for guinea pigs, the usual amounts of virus suspensions sufficed to induce, in a uniform way, typical encephalitis. 2. The opinion previously expressed by Flexner that the guinea pig serves merely to separate weak from strong strains of herpes virus is supported: for only according to the particular method described, could the encephalitogenic power of the Levaditi virus be developed and the weak be converted into a strong herpes strain. With the acquisition of this power, the Levaditi virus acted in precisely the same manner as strong herpes strains both in the guinea pig and the rabbit. Moreover, it was shown in guinea pigs that cross-immunity occurs between weak and strong strains. 3. The two samples of neurovaccine virus employed were incapable of inducing encephalitis in guinea pigs after intracutaneous, intratesticular, corneal, or intracerebral inoculation, although they were actively encephalitogenic in rabbits. In spite of the fact that the vaccine virus and herpes virus are different, as shown by the histopathology and absence of cross-immunity, they behave in the same way when injected into the brain of the guinea pig. The failure of the concomitant action of both viruses to induce encephalitis in the guinea pig suggests that the association of two viruses, under the experimental conditions outlined, is incapable of inducing encephalitis, if either, by itself, is non-encephalitogenic. 4. The serum from normal guinea pigs may neutralize a weak (Levaditi C) but not a strong (H.F.) strain of herpes virus; but the neutralizing action of the serum on Levaditi C virus is not uniform. 5. The Levaditi strain of virus can increase in quantity in the brain of the guinea pig to a degree which permits detection and yet fails to evoke any distinctive clinical picture or definite histopathological changes. 6. Repeated intraperitoneal injections of Levaditi virus in guinea pigs elicit no signs of infection, yet they induce a solid immunity to strong strains of herpes virus.

Optimization of Diagnosis and Treatment of Early Cavities Connected with Herpes Virus Infection

2020 ◽  
Author(s):  
Al'bina Irekovna Bulgakova ◽  
Iuliia Valer'evna Andreeva ◽  
Dinara Madritovna Islamova
Keyword(s):  
Virus Infection ◽  
Herpes Virus ◽  
Diagnosis And Treatment ◽  
Herpes Virus Infection ◽  
Herpès Virus

Réactivations à herpès virus (HSV, CMV) en réanimation : qui et quand traiter ?

2019 ◽  
Vol 28 (3) ◽  
pp. 232-238
Author(s):  
C.-E. Luyt ◽  
G. Hékimian ◽  
N. Bréchot
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Virus ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Charge Virale

Les réactivations à herpès simplex virus (HSV) et à cytomégalovirus (CMV) sont fréquentes chez le patient non immunodéprimé de réanimation. La réactivation HSV est localisée aux voies aériennes ; elle débute au niveau oropharyngé, progresse de façon descendante avec la contamination des voies aériennes distales et peut aboutir, chez certains malades, à une véritable bronchopneumonie herpétique. Elle est en outre associée à un pronostic défavorable. Le traitement prophylactique et préemptif des réactivations HSV ne peut pas être préconisé à l’heure actuelle. Le traitement curatif repose sur un avis d’experts, chez des malades présentant soit une charge virale élevée dans les voies aériennes distales, soit des signes cytologiques d’atteinte parenchymateuse pulmonaire sur les cellules recueillies lors du lavage bronchoalvéolaire. La réactivation CMV sanguine est fréquente et peut être isolée ou associée à une réactivation/atteinte pulmonaire et est aussi associée à un pronostic défavorable. Le traitement prophylactique de la réactivation CMV ne peut pas être préconisé, et le traitement préemptif est en cours d’évaluation. À l’heure actuelle, le traitement curatif des maladies pulmonaires à CMV repose soit sur des signes histologiques d’atteinte pulmonaire, soit sur un faisceau d’arguments clinicobiologiques évoquant une possible maladie à CMV.

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