Japanese Encephalitis remains a significant global health concern, contributing to millions of deaths annually worldwide. Microglial cells, as key innate immune cells within the central nervous system (CNS), exhibit intricate cellular structures and possess molecular phenotypic plasticity, playing pivotal roles in immune responses during CNS viral infections. Particularly under viral inflammatory conditions, microglial cells orchestrate innate and adaptive immune responses to mitigate viral invasion and dampen inflammatory reactions. This review article comprehensively summarizes the pathophysiology of viral invasion into the CNS and the cellular interactions involved, elucidating the roles of various immune mediators, including pro-inflammatory cytokines, in neuroinflammation. Leveraging this knowledge, strategies for modulating inflammatory responses and attenuating hyperactivation of glial cells to mitigate viral replication within the brain are discussed. Furthermore, current chemotherapeutic and antiviral drugs are examined, elucidating their mechanisms of action against viral replication. This review aims to provide insights into therapeutic interventions for Japanese Encephalitis and related viral infections, ultimately contributing to improved outcomes for affected individuals.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s13365-024-01212-z | DOI Listing |
Acute encephalitis syndrome (AES) is a significant public health issue in India, attributed to various etiologies. In eastern Uttar Pradesh, Japanese encephalitis (JE) was the leading cause of AES (10-14% of total AES) until scrub typhus (ST), caused by , was identified in cerebrospinal fluid and blood samples of AES patients contributing more than 60% of AES cases. This study investigates the prevalence of JE-ST coinfection and compares clinical outcomes among JE mono-infection, ST mono-infection, and JE-ST coinfection.
View Article and Find Full Text PDFFEBS J
December 2024
Laboratory of Virology, Regional Centre for Biotechnology, Faridabad, India.
Japanese encephalitis virus (JEV) is the leading causative agent of viral encephalitis in India and contributes to a significant disease burden in South Asian countries. However, no antiviral treatment is available against JEV-induced encephalitis, highlighting the urgent need for novel therapeutic approaches. Repurposing or repositioning drugs was found to be more economical and practical in the current drug development scenario.
View Article and Find Full Text PDFEpidemiol Infect
December 2024
School of Medicine and Dentistry, Griffith University, Gold Coast, Queensland, Australia.
In 2022, the largest ever virgin soil outbreak of Japanese encephalitis (JE) occurred in Australia resulting in 45 reported human cases of JE, with seven fatalities. Japanese encephalitis virus (JEV) was detected in 84 piggeries across Australia. In response, states implemented targeted vaccination programs for those individuals at the highest risk of JEV exposure.
View Article and Find Full Text PDFParasit Vectors
December 2024
Department of Biology, College of Natural Sciences, Kyungpook National University, Daegu, 41566, Republic of Korea.
Background: Culex tritaeniorhynchus, a major vector of Japanese encephalitis virus (JEV), is found across a broad geographical range, including Africa, Asia, Australia and Europe. Understanding the population structure and genetic diversity of pathogen vectors is increasingly seen as important for effective disease control. In China and Japan, two countries in close proximity to the Republic of Korea (ROK), Cx.
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
Animal-derived Food Safety Innovation Team, Anhui Agricultural University, Hefei 230036, China; Anhui Province Key Lab of Veterinary Pathobiology and Disease Control, Anhui Agricultural University, Hefei 230036, China. Electronic address:
Japanese encephalitis caused by Japanese encephalitis virus (JEV) infection leads to the central nervous system disorder in human and swine. Viruses utilize the host protein synthesis mechanisms to efficiently translate their RNAs. Herein, we demonstrated that the host transcription factor SOX10 downregulated an RNA-binding protein heterogeneous nuclear ribonucleoprotein H (HNRNPH1) during JEV infection.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!