Delayed IFN response differentiates replication of West Nile virus and Japanese encephalitis virus in human neuroblastoma and glioblastoma cells

Takamatsu, Yuki; Uchida, Leo; Morita, Kouichi

doi:10.1099/vir.0.000168

Cited by 8 publications

(6 citation statements)

References 20 publications

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“…Astrocytic activation and inflammatory factor release is an important mechanism of Japanese encephalitis virus (10). In vitro cultured glial cells were transfected with the virus, the virus titer was not high, and affected the detection of inflammatory markers (11).…”

Section: Discussionmentioning

confidence: 99%

miR-16-1 expression, heat shock protein 70 and inflammatory reactions in astrocytes of mice with epilepsy induced by encephalitis B virus infection

Yao

Yang

et al. 2017

Experimental and Therapeutic Medicine

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The upregulation of miR-16-1 expression and heat shock protein 70 (HSP70) and inflammatory reaction mechanism in astrocytes of mice with epilepsy induced by encephalitis B virus infection were studied. Six-to-eight-week-old healthy male C57BL/6 mice received intraperitoneal injection of pilocarpine (320–340 mg/kg, 40 mg/ml) to induce status epilepsy. After 7 days, mice were inoculated with 100 µl Dulbecco's modified Eagle's medium (DMEM) in the neck, including 6.25×23 PFU Japanese encephalitis virus P3 wild strain. The experiment was divided into 4 groups, including, the healthy control group, the epilepsy model group, the model group + negative inoculation group and the virus infection group with 10 mice in each group. The healthy control group received intraperitoneal injection of the same amount of normal saline; the model group + negative inoculation group was injected with the same amount of DMEM without P3. One and three days after infection, 5 mice from each group were sacrificed, hippocampus tissues were obtained and astrocytes were isolated. After purification, glial fibrillary acidic protein was identified by immunohistochemical staining. Infected glial cells were detected by P3 antigen of immunofluorescence staining. RT-PCR method was used to detect the expression of miR-16-1 mRNA in astrocytes. Western blot analysis was used to detect the expression of HSP70. ELISA method was used to detect the levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α and nuclear factor-κB (NF-κB) inflammatory factors in tail vein blood. Level of expression of miR-16-1 mRNA, HSP70 as well as IL-6, TNF-α and NF-κB inflammatory factor levels of virus infected mice of 1 and 3 days were significantly higher (P<0.05) than those of model group and negative inoculation group and lowest in control group. In conclusion, the level of expression of miR-16-1 and HSP70 can be increased by the infection of Japanese encephalitis virus on the astrocytes of mice with epilepsy, to promote the expression of IL-6, TNF-α and NF-κB of inflammatory factors.

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Section: Discussionmentioning

confidence: 99%

miR-16-1 expression, heat shock protein 70 and inflammatory reactions in astrocytes of mice with epilepsy induced by encephalitis B virus infection

Yao

Yang

et al. 2017

Experimental and Therapeutic Medicine

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“…However, JEV infection of HeLa cells showed an earlier IFN induction pattern [68]. Additionally, in a more recent study the authors observed that the presence of the viral-derived RNA in the cytoplasm at the early stages of infection, and therefore the timing of IFN induction, depends on the cell type used for their experiment [72]. Altogether, this suggests that differences in RNA leaking from the vesicles to the cytosol among cell lines could be influenced by a cell type-specific conformation of the double-membrane vesicles or other host factors.…”

Section: Antagonism Of Type I Ifn Productionmentioning

confidence: 99%

Antagonism of type I interferon by flaviviruses

Miorin

Maestre

Fernández-Sesma

et al. 2017

Biochemical and Biophysical Research Communications

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The prompt and tightly controlled induction of type I interferon is a central event of the immune defense against viral infection. Flaviviruses comprise a large family of arthropod-borne positive-stranded RNA viruses, many of which represent a serious threat to global human health due to their high rates of morbidity and mortality. All flaviviruses studied so far have been shown to counteract the host’s immune response to establish a productive infection and facilitate viral spread. Here, we review the current knowledge on the main strategies that human pathogenic flaviviruses utilize to escape both type I IFN induction and effector pathways. A better understanding of the specific mechanisms by which flaviviruses activate and evade innate immune responses is critical for the development of better therapeutics and vaccines.

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“…The production of IFN‐α/β through pattern recognition receptors, along with consequent induction of ISG15, is crucial to the control of JEV replication throughout the course of infection. However, the coordinated induction of SOCS expression, along with protein tyrosine phosphatase activity via both JEV nonstructural protein‐related and yet unidentified mechanisms, causes variable efficiency in restricting JEV replication . Results of Western blot have revealed that differentiated PC12 cells were ineffective in inducing tyrosine phosphorylation of Jak1, Stat1 and Stat2 or were able to cause a rapid drop of tyrosine phosphorylation of Jak1, Stat1 and Stat2, as compared to naïve cells after JEV infection.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility of naïve and differentiated PC12 cells to Japanese encephalitis virus infection

Chang

et al. 2017

IUBMB Life

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Japanese encephalitis is a mosquito-borne disease caused by Japanese encephalitis virus (JEV) infection. Although JEV infects and replicates in cells with multiple tissue origins, neurons are the preferential cells for JEV infection. Currently, the identities of JEV cell tropism are largely unclear. To gain better insight into the underlying identities of JEV cell tropism, this study was designed to compare the JEV cell tropism with naïve or differentiated PC12 cells. Through nerve growth factor-differentiated PC12 cells, we discovered that JEV efficiently replicated in differentiated PC12 cells rather than naïve cells. Mechanistic studies revealed that viral adsorption/attachment seemed not to be a crucial factor. Supporting data showed that antagonizing postreceptor intracellular signaling of interferons, along with the activation of suppressor of cytokine signaling-3 (SOCS3) expression and protein tyrosine phosphatase activity, were apparent in differentiated PC12 cells after JEV infection. Independent of differentiating inducing agents, the upregulation of SOCS3 expression and protein tyrosine phosphatase activity, as well as preferential JEV tropism, were common in JEV-infected differentiated PC12 cells. Using cultured primary neurons, JEV efficiently replicated in embryonic neurons rather than adult neurons, and the preference was accompanied by higher SOCS3 expression and protein tyrosine phosphatase activity. Given that both SOCS3 and protein tyrosine phosphatases have been implicated in the process of neuronal differentiation, JEV infection seems to not only create an antagonizing strategy to escape host's interferon antiviral response but also takes advantage of cellular machinery to favor its replication. Taken together, current findings imply that dynamic changes within cellular regulators of antiviral machinery could be accompanied by events of neuronal differentiation, thus concurrently playing roles in the control of JEV cell tropism and replication. © 2017 IUBMB Life, 69(2):79-87, 2017.

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Delayed IFN response differentiates replication of West Nile virus and Japanese encephalitis virus in human neuroblastoma and glioblastoma cells

Cited by 8 publications

References 20 publications

miR-16-1 expression, heat shock protein 70 and inflammatory reactions in astrocytes of mice with epilepsy induced by encephalitis B virus infection

miR-16-1 expression, heat shock protein 70 and inflammatory reactions in astrocytes of mice with epilepsy induced by encephalitis B virus infection

Antagonism of type I interferon by flaviviruses

Susceptibility of naïve and differentiated PC12 cells to Japanese encephalitis virus infection

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