Japanese Encephalitis: A Tale of Inflammation and Degeneration in the Central Nervous System

Dutta, Kallol; Basu, Anirban

doi:10.1007/978-1-4939-1071-7_15

Cited by 4 publications

(3 citation statements)

References 170 publications

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“…These illnesses occur in a bimodal distribution, affecting the very young or nonimmune visitors to endemic regions, and the elderly, whose immunity has waned. The neuropathology of JEVand MVEV involves neuronal damage and inflammatory infiltrates, and viral antigen may be detected within neurons of the thalamus, hippocampus, substantia nigra and medulla oblongata [58,59].…”

Section: Flaviviridaementioning

confidence: 99%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus-and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

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Section: Flaviviridaementioning

confidence: 99%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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“…In many cases, promising drugs/molecules that have been found to be efficacious in in vitro or in vivo animal models either were not deemed suitable for or failed to replicate their success in actual human trials. Supplementary Table 1 (an updated version of a similar table in a book chapter by the same authors 32 ) gives a detailed list of all those drugs/molecules that have been reported to date to counter JE in various models of the disease. Clinical trials involving administration of dexamethasone 33 , interferon alpha 2a 34 , and ribavirin 35 were not successful.…”

Section: Therapeutic Approach To Japanese Encephalitis: Dark Clouds Wmentioning

confidence: 99%

Recent advances in Japanese encephalitis

Basu

Dutta

2017

F1000Res

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Japanese encephalitis is a flaviviral disease that is endemic to the South, Southeast Asia, and Asia Oceania regions. Given that about 60% of the world’s population (about 7.4 billion) resides in this region (about 4.4 billion), this disease poses a significant threat to global health. Active vaccination campaigns conducted in endemic countries have led to a decrease in the number of reported cases over the years. In this article, we strive to briefly highlight recent advances in understanding the role of microRNAs in disease pathology, focus on providing brief summaries of recent clinical trials in the field of Japanese encephalitis therapeutics, and review the current prophylactic strategies.

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“…JEV is one of the mosquito-borne flaviviruses and is transmitted by culex. After the host is bitten by a mosquito infected with JEV, the virus begins to replicate, migrates through the periphery, such as draining lymph nodes, spleen, and kidney, and even crossing the blood-brain barrier (BBB) into the CNS ( King et al, 2007 ; Dutta and Basu, 2014 ). Bovine and water birds amplify host supply virus in the blood for feeding mosquitoes, and finally, JEV infects dead-end host humans ( Turtle and Solomon, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

The Infection of the Japanese Encephalitis Virus SA14-14-2 Strain Induces Lethal Peripheral Inflammatory Responses in IFNAR Deficiency Mice

et al. 2022

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The Japanese encephalitis virus (JEV) is a leading cause of mosquito-borne viral encephalitis worldwide. Clinical symptoms other than encephalitis, on the other hand, are substantially more prevalent with JEV infection, demonstrating the relevance of peripheral pathophysiology. We studied the peripheral immunopathogenesis of JEV using IFNAR deficient (IFNAR–/–) mice infected with the SA14-14-2 strain under the BSL-2. The body weight and survival rate of infected-IFNAR–/–mice decreased significantly. Infected-IFNAR–/–mice’s liver and spleen demonstrated obvious tissue damage and inflammatory cell infiltration. There was also extensive viral replication in the organs. IFN-α/β protein expression was dramatically elevated in peripheral tissues and serum, although the related interferon-stimulated genes (ISGs) remained low in the spleen and liver of infected-IFNAR–/–animals. Consistently, the differentially expressed genes (DEGs) analysis using RNA-sequencing of spleens showed inflammatory cytokines upregulation, such as IL-6, TNF-α, and MCP-1, and IFN-γ associated cytokine storm. The infiltration of macrophages and neutrophils in the spleen and liver of SA14-14-2-infected IFNAR–/– mice was dramatically elevated. However, there was no significant difference in tissue damage, viral multiplication, or the production of IFNα/β and inflammatory cytokines in the brain. Infection with the JEV SA14-14-2 strain resulted in a lethal peripheral inflammatory response and organ damage without encephalitis in IFNAR–/– mice. Our findings may help shed light on the peripheral immunopathogenesis associated with clinical JEV infection and aid in developing treatment options.

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Japanese Encephalitis: A Tale of Inflammation and Degeneration in the Central Nervous System

Cited by 4 publications

References 170 publications

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Recent advances in Japanese encephalitis

The Infection of the Japanese Encephalitis Virus SA14-14-2 Strain Induces Lethal Peripheral Inflammatory Responses in IFNAR Deficiency Mice

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