instruction:
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
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C57 strain mice were inoculated intraperitoneally with denatured mouse hepatitis virus strain 3 particles and virus surface projection, membrane and ribonucleoprotein subeomponents, obtained from detergent treated purified virus preparations. All immunised animals developed high levels of serum antibody directed against the respective antigens, detectable by enzyme-linked immunosorbent assay. Mice that had been immunised with denatured virus particles or surface projections were protected against infection with mouse hepatitis virus strain 3, whereas immunisation with virus membrane or ribonucleoprotein subcomponents failed to protect mice against virus challenge.
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Archives of Virology Antigenieity of Mouse Hepatitis Virus Strain 3 Subeomponents in C57 Strain Miee


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We report a hereditary leukodystrophy in Standard Schnauzer puppies. Clinical signs occurred shortly after birth or started at an age of under 4 weeks and included apathy, dysphoric vocalization, hypermetric ataxia, intension tremor, head tilt, circling, proprioceptive deficits, seizures and ventral strabismus consistent with a diffuse intracranial lesion. Magnetic resonance imaging revealed a diffuse white matter disease without mass effect. Macroscopically, the cerebral white matter showed a gelatinous texture in the centrum semiovale. A mild hydrocephalus internus was noted. Histopathologically, a severe multifocal reduction of myelin formation and moderate diffuse edema without inflammation was detected leading to the diagnosis of leukodystrophy. Combined linkage analysis and homozygosity mapping in two related families delineated critical intervals of approximately 29 Mb. The comparison of whole genome sequence data of one affected Standard Schnauzer to 221 control genomes revealed a single private homozygous protein changing variant in the critical intervals, TSEN54:c.371G>A or p.(Gly124Asp). TSEN54 encodes the tRNA splicing endonuclease subunit 54. In humans, several variants in TSEN54 were reported to cause different types of pontocerebellar hypoplasia. The genotypes at the c.371G>A variant were perfectly associated with the leukodystrophy phenotype in 12 affected Standard Schnauzers and almost 1000 control dogs from different breeds. These results suggest that TSEN54:c.371G>A causes the leukodystrophy. The identification of a candidate causative variant enables genetic testing so that the unintentional breeding of affected Standard Schnauzers can be avoided in the future. Our findings extend the known genotype-phenotype correlation for TSEN54 variants. Various hereditary diseases of the cerebral white matter occur in humans and dogs. We describe a new leukodystrophy in Standard Schnauzers. Genetic mapping and whole genome sequence analysis identified a likely candidate causative variant in the TSEN54 gene encoding tRNA splicing endonuclease 54. These results provide new information about the role of TSEN54 in cell metabolism and the development of the central nervous system in the late gestational and early post-natal period. The affected dogs potentially represent a translational large animal model for similar leukoencephalopathies in human medicine. The clinical phenotype in Schnauzers included multifocal central nervous system signs. A holistic pathogenically driven understanding of disease initiation and perpetuation requires a solid analysis of the underlying genetics and characterization of the disease phenotype at the clinical and cellular as well as sub-cellular level. In contrast to the canine phenotype with a predominant manifestation in the cerebrum white matter, other TSEN54 variants in humans have been reported to result in a different pathological phenotype characterized by pontocerebellar hypoplasia. The differences between humans and dogs underscore the need for comparative analysis at the clinical, pathological and molecular level to understand species-specific protein mediated pathways, interactions and outcomes.
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TSEN54 missense variant in Standard Schnauzers with leukodystrophy Author summary


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emetine, and homoharringtonine inhibit SARS-CoV-2 replication in vitro, Antiviral Research, https://doi. ABSTRACT An escalating pandemic by the novel SARS-CoV-2 virus is impacting global health and effective therapeutic options are urgently needed. We evaluated the in vitro antiviral effect of compounds that were previously reported to inhibit coronavirus replication and compounds that are currently under evaluation in clinical trials for SARS-CoV-2 patients. We report the antiviral effect of remdesivir, lopinavir, homorringtonine, and emetine against SARS-CoV-2 virus in Vero E6 cells with the estimated 50% effective concentration at 23.15 µM, 26.63 µM, 2.55 µM and 0.46 µM, respectively. Ribavirin or favipiravir that are currently evaluated under clinical trials showed no inhibition at 100 µM. Synergy between remdesivir and emetine was observed, and remdesivir at 6.25 µM in combination with emetine at 0.195 µM may achieve 64.9% inhibition in viral yield. Combinational therapy may help to reduce the effective concentration of compounds below the therapeutic plasma concentrations and provide better clinical benefits.
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Journal Pre-proof Remdesivir, lopinavir, emetine, and homoharringtonine inhibit SARS-CoV-2 replication in vitro SHORT COMMUNICATION Remdesivir, lopinavir, emetine, and homoharringtonine inhibit SARS-CoV-2 replication in vitro