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.
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. 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.
The neuronal damage and host immune responses triggered by viral reactivations are believed to contribute to long-term neurodegeneration. To investigate the causes of response variations, Szpara and her investigative team infected human neuronal cells with 1 of 3 HSV-1 strains that are known to differ in their ability to cause disease in the nervous system. Next, they used deep sequencing to identify and quantify the transcriptomes of the neurons during infection by HSV According to the study, when a neuronal cell is infected with HSV-1, the resulting transcriptome includes the entire collection of mRNAs produced by both the human neuron and the HSV-1 virus.
By analyzing the timing and amount of mRNAs expressed during infection, scientists can gain insights on the proteins that will soon be produced. The viral proteins and new viral progeny produced during infection ultimately lead to health problems. The investigators also used immunofluorescence staining of neurons and Western blotting for viral protein cells to observe the outcomes of viral and host gene expression.
Additionally, they used scanning electron microscopy to directly observe changes in neuronal morphology during infection. Credit: Colleen Mangold, Penn State. Explore further. More information: Colleen A. Mangold et al, Viral infection of human neurons triggers strain-specific differences in host neuronal and viral transcriptomes, PLOS Pathogens DOI: Provided by Pennsylvania State University.
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