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Research
Changqin Gu
Huazhong Agriculture University
Corresponding Author
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Background
Japanese Encephalitis (JE) is a zoonotic natural epidemic disease caused by Japanese Encephalitis Virus (JEV) infection. Currently, there is no specific medicine for Japanese encephalitis. Autophagy is a lysosomal degradation process that plays an important role in viral infection and cellular immunity. In vitro studies have shown that the Japanese encephalitis virus replication mechanism is related to the autophagy pathway. We hope that by studying the effects of autophagy-regulating drugs on JEV infection and host response in mice, will provide effective clinical trials for autophagy-regulating drugs in the treatment of Japanese encephalitis and other viral infectious diseases.
Methods
After establishing appropriate animal model. We observed the neurological symptoms of the mice and counted their survival rate. We observed histopathological changes in brain tissues of mice. We compared the extent of neuroinflammatory responses in the brain of mice and explored the signaling processes involved in neuroinflammation.
Results
We found autophagy inhibitors wortmannin (Wort) and chloroquine (CQ) slow down the occurrence of neurological symptoms and reduce the prevalence of JEV-infected mice. As expected, autophagy inhibitors can inhibit the activation of the PI3K/AKT/NF-kB pathway to alleviate cerebral inflammatory responses in mice, thereby protecting the mice from JEV-induced death.
Conclusions
Our study suggests that autophagy inhibitors wortmannin and chloroquine could attenuate the inflammatory response in the brain of JEV infected mice, providing a clinical basis for the treatment of Japanese encephalitis
Keywords
autophagy inhibitor, Japanese encephalitis virus, mice, encephalitis
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A new preprint design is coming!
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Changqin Gu
Huazhong Agriculture University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 08 May, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Neurobiology of Disease
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Japanese Encephalitis (JE) is a zoonotic natural epidemic disease caused by Japanese Encephalitis Virus (JEV) infection. Currently, there is no specific medicine for Japanese encephalitis. Autophagy is a lysosomal degradation process that plays an important role in viral infection and cellular immunity. In vitro studies have shown that the Japanese encephalitis virus replication mechanism is related to the autophagy pathway. We hope that by studying the effects of autophagy-regulating drugs on JEV infection and host response in mice, will provide effective clinical trials for autophagy-regulating drugs in the treatment of Japanese encephalitis and other viral infectious diseases.
Methods
After establishing appropriate animal model. We observed the neurological symptoms of the mice and counted their survival rate. We observed histopathological changes in brain tissues of mice. We compared the extent of neuroinflammatory responses in the brain of mice and explored the signaling processes involved in neuroinflammation.
Results
We found autophagy inhibitors wortmannin (Wort) and chloroquine (CQ) slow down the occurrence of neurological symptoms and reduce the prevalence of JEV-infected mice. As expected, autophagy inhibitors can inhibit the activation of the PI3K/AKT/NF-kB pathway to alleviate cerebral inflammatory responses in mice, thereby protecting the mice from JEV-induced death.
Conclusions
Our study suggests that autophagy inhibitors wortmannin and chloroquine could attenuate the inflammatory response in the brain of JEV infected mice, providing a clinical basis for the treatment of Japanese encephalitis
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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