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Inapparent viral infection of cells in vitro. 3. Manifestations of infection of L mouse cells by Japanese encephalitis virus 总被引:2,自引:0,他引:2
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Dubbs, D. R. (University of Minnesota, Minneapolis), and W. F. Scherer. Inapparent viral infection of cells in vitro. III. Manifestations of infection of L mouse cells by Japanese encephalitis virus. J. Bacteriol. 91:2349-2355. 1966.-Nine strains of Japanese encephalitis (JE) virus were propagated serially in cultures of L cells reaching titers of 10(3.5) to 10(6.3). Although cytopathic effects were not seen in cultures of contiguous L cells after infection with JE virus, cell growth was inhibited. Moreover, cell destruction was readily apparent in infected cultures of sparse, noncontiguous L cells. Differences in the size of cell population of infected and noninfected cultures (i) occurred despite only 0.2 to 3.5% of the cells in infected cultures being associated with infectious virus, (ii) were greater in actively growing cultures than in those kept in maintenance media, and (iii) were probably in part related to an interferon produced in infected cultures. 相似文献
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Yu-Fen Tseng Chien-Chih Wang Shuen-Kuei Liao Ching-Kai Chuang Wei-June Chen 《Journal of biomedical science》2011,18(1):20
Japanese encephalitis (JE) virus is the most common cause of epidemic viral encephalitis in the world. The virus mainly infects
neuronal cells and causes an inflammatory response after invasion of the parenchyma of the brain. The death of neurons is
frequently observed, in which demyelinated axons are commonly seen. The mechanism that accounts for the occurrence of demyelination
is ambiguous thus far. With a mouse model, the present study showed that myelin-specific antibodies appeared in sera, particularly
in those mice with evident symptoms. Meanwhile, specific T cells proliferating in response to stimulation by myelin basic
protein (MBP) was also shown in these mice. Taken together, our results suggest that autoimmunity may play an important role
in the destruction of components, e.g., MBP, of axon-surrounding myelin, resulting in demyelination in the mouse brain after infection with the JE virus. 相似文献
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Dengyuan Zhou Fan Jia Qiuyan Li Luping Zhang Zheng Chen Zikai Zhao Min Cui Yunfeng Song Huanchun Chen Shengbo Cao Jing Ye 《中国病毒学》2018,33(6):515-523
Japanese encephalitis virus(JEV) is a mosquito-borne virus and the major cause of viral encephalitis in Asia. NS1', a52-amino acid C-terminal extension of NS1, is generated with a-1 programmed ribosomal frameshift and is only present in members of the Japanese encephalitis serogroup of flaviviruses. Previous studies demonstrated that NS1' plays a vital role in virulence, but the mechanism is unclear. In this study, an NS1' defected(rG66A) virus was generated. We found that rG66A virus was less virulent than its parent virus(pSA14) in wild-type mice. However, similar mortality caused by the two viruses was observed in an IFNAR knockout mouse model. Moreover, we found that rG66A virus induced a greater type Ⅰ interferon(IFN) response than that by pSA14, and JEV NS1' significantly inhibited the production of IFN-b and IFN-stimulated genes. Taken together, our results reveal that NS1' plays a vital role in blocking type I IFN production to help JEV evade antiviral immunity and benefit viral replication. 相似文献
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Wei Han Mingxing Gao Changqing Xie Jinhua Zhang Zikai Zhao Xueying Hu Wanpo Zhang Xiaoli Liu Shengbo Cao Guofu Cheng Changqin Gu 《PLoS neglected tropical diseases》2021,15(6)
Japanese encephalitis virus (JEV) is a pathogen that causes severe vector-borne zoonotic diseases, thereby posing a serious threat to human health. Although JEV is potentially neurotropic, its pathogenesis and distribution in the host have not been fully elucidated. In this study, an infected mouse model was established using a highly virulent P3 strain of JEV. Immunohistochemistry and in situ hybridization, combined with anatomical imaging of the mouse brain, were used to dynamically localize the virus and construct three-dimensional (3D) images. Consequently, onset of mild clinical signs occurred in some mice at 3.5 d post JEV infection, while most mice displayed typical neurological signs at 6 d post-infection (dpi). Moreover, brain pathology revealed typical changes associated with non-suppurative encephalitis, which lasted up to 8 d. The earliest detection of viral antigen was achieved at 3 dpi in the thalamus and medulla oblongata. At 6 dpi, the positive viral antigen signals were mainly distributed in the cerebral cortex, olfactory area, basal ganglia, thalamus, and brainstem regions in mice. At 8 dpi, the antigen signals gradually decreased, and the localization of JEV tended to concentrate in the cerebrum and thalamus, while no viral antigen was detected in the brain at 21 dpi. In this model, the viral antigen was first expressed in the reticular thalamic nucleus (Rt), and the virus content is relatively stable. The expression of the viral antigen in the hippocampal CA2 region, the anterior olfactory nucleus, and the deep mesencephalic nucleus was high and persistent. The 3D images showed that viral signals were mostly concentrated in the parietal cortex, occipital lobe, and hippocampus, near the mid-sagittal plane. In the early stages of infection in mice, a large number of viral antigens were detected in denatured and necrotic neurons, suggesting that JEV directly causes neuronal damage. From the time of its entry, JEV is widely distributed in the central nervous system thereby causing extensive damage. 相似文献
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Molecular basis for attenuation of neurovirulence of a yellow fever Virus/Japanese encephalitis virus chimera vaccine (ChimeriVax-JE) 总被引:3,自引:0,他引:3
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Arroyo J Guirakhoo F Fenner S Zhang ZX Monath TP Chambers TJ 《Journal of virology》2001,75(2):934-942
A yellow fever virus (YFV)/Japanese encephalitis virus (JEV) chimera in which the structural proteins prM and E of YFV 17D are replaced with those of the JEV SA14-14-2 vaccine strain is under evaluation as a candidate vaccine against Japanese encephalitis. The chimera (YFV/JEV SA14-14-2, or ChimeriVax-JE) is less neurovirulent than is YFV 17D vaccine in mouse and nonhuman primate models (F. Guirakhoo et al., Virology 257:363-372, 1999; T. P. Monath et al., Vaccine 17:1869-1882, 1999). Attenuation depends on the presence of the JEV SA14-14-2 E protein, as shown by the high neurovirulence of an analogous YFV/JEV Nakayama chimera derived from the wild JEV Nakayama strain (T. J. Chambers, A. Nestorowicz, P. W. Mason, and C. M. Rice, J. Virol. 73:3095-3101, 1999). Ten amino acid differences exist between the E proteins of ChimeriVax-JE and the YFV/JEV Nakayama virus, four of which are predicted to be neurovirulence determinants based on various sequence comparisons. To identify residues that are involved in attenuation, a series of intratypic YFV/JEV chimeras containing either single or multiple amino acid substitutions were engineered and tested for mouse neurovirulence. Reversions in at least three distinct clusters were required to restore the neurovirulence typical of the YFV/JEV Nakayama virus. Different combinations of cluster-specific reversions could confer neurovirulence; however, residue 138 of the E protein (E(138)) exhibited a dominant effect. No single amino acid reversion produced a phenotype significantly different from that of the ChimeriVax-JE parent. Together with the known genetic stability of the virus during prolonged cell culture and mouse brain passage, these findings support the candidacy of this experimental vaccine as a novel live-attenuated viral vaccine against Japanese encephalitis. 相似文献
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Summary When MM and Columbia SK virus were propagated in the chick embryo, the virus disappeared from the allantoic fluid and from the embryonic brain tissue after 6 to 9 chorioallantoic passages. Amniotic passages, however, resulted in a gradual increase of the mouse infectivity titre of the amniotic fluid and of the fluid of the regularly observed subcutaneous edema of the embryos, though after 22 passages the ID50 titre was still 3 logs lower than that of the original mouse brain suspension. The virus was present not only in amniotic fluid, but also in allantoic fluid and throughout the whole embryo. In spite of the pretty high mouse infectivity titres, the extra-embryonic fluids failed to produce haemagglutination of sheep red cells, whereas low haemagglutination titres could be obtained with suspensions of embryonic brain tissue. No evidence was obtained, that a non-specific inhibitor was responsible for the inability to produce haemagglutination. The virus present in egg fluids is only partially adsorbed, which is in contrast with the almost complete adsorption of virus in mouse brain suspension. The adsorption of a relatively small amount of virus might be one of the factors responsible for lack of haemagglutinating ability. It is suggested, that another coinciding factor, which is necessary for the initiation of the haemagglutination might be present in the central nervous system lesion.Third publication: Antonie van Leeuwenhoek17, 137, 1951. 相似文献
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Single cell clones of latently infected mouse neuroblastoma cells were isolated from a culture chronically infected with mouse hepatitis virus in the presence of an antiviral antibody. These cell clones did not produce infections virus or exhibit viral cytopathic effects during cultivation at 32, 37, or 39°C. Infectious virus was isolated from single cell clones via fusion with permissive cells using polyethylene glycol, but not after fusion with inactivated Sendai virus or following treatment with metabolic inhibitors. One cell clone (S-3) from which virus was rescued was negative for viral antigen by immunofluorescence. The S-3 cell clone and no demonstrable virus antigen by complement-fixation tests using cytoplasmic extracts or virus-specified proteins detectable by polyacrylamide gel electrophoresis. The rescued viruses exhibited a temperature dependent growth defect at 32°C and have been classified as cold sensitive mutants. This study suggests that a complete genome of a positive stranded RNA virus can remain latent in infected cells without the expression of detectable virus antigen. 相似文献
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The changes in monoamine levels of different brain regions following Japanese encephalitis virus (JEV) intraperitoneal inoculation were examined in experimentally JEV-infected mice. In addition, virus distribution was studied using infectivity assay and immuno-histochemistry of viral antigen. 1) The level of monoamines in brain tissues was not affected by 48 hours after viral inoculation, but marked effects were elicited at 96 hours after the inoculation. The cerebral concentration of 5-hydroxyindole-3-acetic acid (5 HIAA) was increased, while that of dopamine (DA) showed a decrease. Especially these alteration were observed in the cerebral cortex, but not in the cerebellum. 2) The viral growth in the brain was observed at 48 hours after the inoculation. The growth in the cerebellum, however, was found to be lower than those in other cerebral regions. 3) The viral antigen was detected in the cerebral cortex, hippocampus, mesencephalon and diencephalon in addition to the substantia nigra and striatum. From these results, it is presumed that clinical manifestation of JEV infection may involve the changes in the metabolism of neurotransmitter, especially those of DA and serotonin in the brain. 相似文献
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While a number of studies have documented the importance of microglia in central nervous system (CNS) response to injury, infection and in disease state, little is known regarding how the neuronal death initiates the cascades of secondary neuroinflammation. We have exploited an experimental model of Japanese encephalitis to better understand how neuronal death following viral infection initiates microglial activation following Japanese encephalitis virus infection. We have earlier shown that the altered expression of tumor necrosis factor receptor-1 (TNFR-1) and TNFR associated death domain (TRADD) following Japanese encephalitis virus infection regulates the downstream apoptotic cascades. Here we have reported that silencing TRADD expression with small-interfering RNA reduced neuronal apoptosis and subsequent microglial and astroglial activation and release of various pro-inflammatory mediators. Our findings suggest that the engagement of TNFR-1 and TRADD following Japanese encephalitis virus infection plays a crucial role in glial activation also and influences the outcome of viral pathogenesis. 相似文献
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Venezuelan equine encephalitis (VEE) virus is a mosquito-borne alphavirus associated with sporadic outbreaks in human and equid populations in the Western Hemisphere. After the bite of an infected mosquito, the virus initiates a biphasic disease: a peripheral phase with viral replication in lymphoid and myeloid tissues, followed by a neurotropic phase with infection of central nervous system (CNS) neurons, causing neuropathology and in some cases fatal encephalitis. The mechanisms allowing VEE virus to enter the CNS are currently poorly understood. Previous data have shown that the virus gains access to the CNS by infecting olfactory sensory neurons in the nasal mucosa of mice. However, at day 5 after inoculation, the infection of the brain is multifocal, indicating that virus particles are able to cross the blood-brain barrier (BBB). To better understand the role of the BBB during VEE virus infection, we used a well-characterized mouse model system. Using VEE virus replicon particles (VRP), we modeled the early events of neuroinvasion, showing that the replication of VRP in the nasal mucosa induced the opening of the BBB, allowing peripherally administered VRP to invade the brain. Peripheral VEE virus infection was characterized by a biphasic opening of the BBB. Further, inhibition of BBB opening resulted in a delayed viral neuroinvasion and pathogenesis. Overall, these results suggest that VEE virus initially enters the CNS through the olfactory pathways and initiates viral replication in the brain, which induces the opening of the BBB, allowing a second wave of invading virus from the periphery to enter the brain. 相似文献
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Clonal analysis of mammalian cell cultures persistently infected with Japanese encephalitis virus.
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More than 200 cells were cloned from populations of mammalian cells persistently infected with Japanese encephalitis virus. Only four cloned cultures contained cells that had viral antigen measurable by immunofluorescence and that released infectious virus, yet all clones harbored virus-specific RNA. Superinfection of cloned cells with wild-type Japanese encephalitis virus did not produce cytopathic effects, but resulted in production of viral antigen and infectious virus in formerly nonproducing clones. Cocultivation of nonproducer clone cells with normally permissive cells did not induce virus production, nor did treatment of nonproducer clones with various inhibitors of DNA, RNA, or protein synthesis. It is suggested that the cloning procedure may have selected for a particular subpopulation of cells and that defective virus is also involved in establishment and maintenance of persistent infection. 相似文献
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Li Mengyuan Yang Jiali Ye Chuantao Bian Peiyu Yang Xiaofei Zhang Haijun Luo Chuanyu Xue Zhifeng Lei Yingfeng Lian Jianqi 《中国病毒学》2021,36(6):1554-1565
Virologica Sinica - Japanese encephalitis virus (JEV) is a leading cause of viral encephalitis in endemic regions of Asia. The neurotropism of JEV and its high-efficiency replication in neurons are... 相似文献
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High viral load in the cerebrospinal fluid and brain correlates with severity of simian immunodeficiency virus encephalitis
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Zink MC Suryanarayana K Mankowski JL Shen A Piatak M Spelman JP Carter DL Adams RJ Lifson JD Clements JE 《Journal of virology》1999,73(12):10480-10488
AIDS dementia and encephalitis are complications of AIDS occurring most frequently in patients who are immunosuppressed. The simian immunodeficiency virus (SIV) model used in this study was designed to reproducibly induce AIDS in macaques in order to examine the effects of a neurovirulent virus in this context. Pigtailed macaques (Macaca nemestrina) were coinoculated with an immunosuppressive virus (SIV/DeltaB670) and a neurovirulent molecularly cloned virus (SIV/17E-Fr), and more than 90% of the animals developed moderate to severe encephalitis within 6 months of inoculation. Viral load in plasma and cerebrospinal fluid (CSF) was examined longitudinally to onset of AIDS, and viral load was measured in brain tissue at necropsy to examine the relationship of systemic and central nervous system (CNS) viral replication to the development of encephalitis. In all animals, plasma viral load peaked at 10 to 14 days postinfection and remained high throughout infection with no correlation found between plasma viremia and SIV encephalitis. In contrast, persistent high levels of CSF viral RNA after the acute phase of infection correlated with the development of encephalitis. Although high levels of viral RNA were found in the CSF of all macaques (six of six) during the acute phase, this high level was maintained only in macaques developing SIV encephalitis (five of six). Furthermore, the level of both viral RNA and antigen in the brain correlated with the severity of the CNS lesions. The single animal in this group that did not have CNS lesions had no detectable viral RNA in any of the regions of the brain. The results substantiate the use of CSF viral load measurements in the postacute phase of SIV infection as a marker for encephalitis and CNS viral replication. 相似文献
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Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus,which causes the most commonly diagnosed viral encephalitis named Japanese encephalitis (JE) in the world with an unclear pathogenesis.Axl,a receptor tyrosine kinase from TAM family,plays crucial role in many inflammatory diseases.We have previously discovered that Axl deficiency resulted in more severe body weight loss in mice during JEV infection,which we speculate is due to the anti-inflammatory effect of Axl during JE.Currently,the role of Axl in regulating the neuroinflammation and brain damage during JE has not been investigated yet.In this study,by using Axl deficient and heterozygous control mice,we discovered that Axl deficient mice displayed accelerated JE progression and exacerbated brain damage characterized by increased neural cell death,extended infiltration of inflammatory cells,and enhanced production of pro-inflammatory cytokines,in comparison to control mice.Additionally,consistent with our previous report,Axl deficiency had no impact on the infection and target cell tropism of JEV in brain.Taken together,our results suggest that Axl plays an anti-inflammatory and neuroprotective role during the pathogenesis of JE. 相似文献
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In a previously well child with no evidence of pre-existing immunologic defect a fatal encephalitis developed 10 days after administration of measles vaccine. There was pathologic evidence of an early viral encephalitis characterized by perivascular mononulcear infiltrates. Although the virus was not recovered, the diagnosis of a measles virus infection and encephalitis is supported by the postmortem findings of Warthin-Finkeldey cells in lymphoid tissues, an intranuclear inclusion in the brain and histologic changes of encephalitis. 相似文献
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David J. Giron 《Applied microbiology》1969,18(4):584-588
MM virus propagated in mouse brain replicates to low titers in L cells without production of cytopathic effect (CPE). After growing the virus in BHK-21 cells, however, the virus replicates to high titers in L cells with complete CPE. It was found that suspensions of MM virus propagated in L cells directly from the mouse brain contained much more interferon than did suspensions of virus which had first been grown in BHK-21 cells. Mouse brain suspensions of the virus were also found to contain high interferon titers. Treatment of L cells with actinomycin D before infection with mouse brain-grown virus resulted in full virus replication with CPE. BHK-21 cell-grown virus diluted in L cell interferon behaved like mouse brain-grown virus in L cells. It is concluded that the presence of interferon in the inoculum is largely responsible for the suppression of MM virus replication in L cells. 相似文献