• IMMUNE NETWORK
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• v.12 no.2
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• pp.48-57
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• 2012

Acute viral encephalitis caused by neurotrophic viruses, such as mosquito-borne flaviviruses, is an emerging and re-emerging disease that represents an immense global health problem. Considerable progression has been made in understanding the pathogenesis of acute viral encephalitis, but the immune-pathological processes occurring during the progression of encephalitis and the roles played by various molecules and cellular components of the innate and adaptive systems still remain undefined. Recent findings reveal the significant contribution of Toll-like receptors (TLRs) and regulatory $CD4^+$ T cells in the outcomes of infectious diseases caused by neurotrophic viruses. In this review, we discuss the ample evidence focused on the roles of TLRs and $CD4^+$ helper T cell subsets on the progression of acute viral encephalitis. Finally, we draw attention to the importance of these molecules and cellular components in defining the pathogenesis of acute viral encephalitis, thereby providing new therapeutic avenues for this disease.

• Annals of Clinical Neurophysiology
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• v.11 no.1
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• pp.33-36
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• 2009

Bickerstaff's brainstem encephalitis (BBE) is an autoimmune central nervous system disorder. It can occur in more limited forms and may overlap with Guillain-Barr$\acute{e}$ syndrome (GBS). A 49-year-old female presented with rapidly progressive paralytic ileus, urinary retention, deep drowsiness, ophthalmoplegia, dysarthria, ataxia, quadriparesis and hyporeflexia after viral meningitis. She was diagnosed as BBE with GBS and treated with immunoglobulin. She was completely recovered after 1 month. It is a rare case of BBE overlapping with GBS presenting with severe paralytic ileus.

• Proceedings of the Microbiological Society of Korea Conference
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• 2000.05a
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• pp.23-36
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• 2000

Japanese encephalitis virus (JEV) is the causative agent of a mosquito-borne encephalitis and is transmitted to human via persistently infected mosquito vectors. Although the virus is known to cause only acute infection, there were reports that showed neurological sequelae, latent infection in peripheral mononuclear cells, and recurrence of the disease after acute encephalitis. Innate resistance of certain cell lines, abnormal SN1 expression of the virus, and anti-apoptotic effect of cullular bcl-2 have been suggested as probable causes of JEV persistence even in the absence of defective interfering (DI) particles. Although possible involvement of DI particles in JEV persistence was suggested, neither has a direct evidence for DI presence nor its molecular characterization been made. Two questions asked in this study are whether the DI virus plays any role in JEV persistent infection if it is associated with and what type of change(s) can be made in persistently infected cells to avoid apoptosis even with the continuous virus replication, DI-free standard stock of JEV was infected in BHK-21, Vero, and SW13 cells and serial high multiplicity passages were performed in order to generate DI particles. There different-sized DI RNA species which were defective in both structural and nonstructural protein coding genes. Rescued ORFs of the DI genome maintained in-frame and the presence of replicative intermediate or replicative form RNA of the DI particles confirmed their replication competence. On the other hand, several clones with JEV persistent infection were established from the cells survived acute infections during the passages. Timing of the DI virus generation during the passages seemed coincide to the appearance of persistently infected cells. The DI RNAs were identified in most of persistently infected cells and were observed throughout the cell maintenance. One of the cloned cell line maintained the viral persistence without DI RNA coreplication. The cells with viral persistence released the reduced but continuous infectious JEV particle for up to 9 months and were refractory to homologous virus superinfection but not to heterologous challenges. Unlike the cells with acute infection these cells were devoid of characteristic DNA fragmentation and JEV-induced apoptosis with or without homologous superinfection. Therefore, the DI RNA generated during JEV undiluted serial passage on mammalian cells was shown to be biologically active and it seemed to be responsible, at least in part, for the establishment and maintenance of the JEV persistence in mammalian cells. Viral persistence without DI RNA coreplication, as in one of the cell clones, supports that JEV persistent infection could be maintained with or without the presence of DI particles. In addition, the fact that the cells with JEV persistence were resistant against homologous virus superinfection, but not against heterologous one, suggests that different viruses have their own and independent pathway for cytopathogenesis even if viral cytopathic effect could be converged to an apoptosis after all.

• Investigative Magnetic Resonance Imaging
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• v.20 no.4
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• pp.250-253
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• 2016

Acute Japanese encephalitis (JE) is an endemic viral infectious disease in various parts of Far East and Southeast Asian countries including Korea. Bilateral thalami are the most common involving sites in JE. Other areas including the basal ganglia, substantia nigra, red nucleus, pons, cerebral cortex and cerebellum may be also involved. We report an extremely unusual brain diffusion-weighted MR imaging (DWI) findings in a 53-year-old man with serologically proven JE involving unilateral deep gray matter and temporal lobe, which shows multifocal high signal intensities in left thalamus, left substantia nigra, left caudate nucleus and left medial temporal cortex on T2-weighted image and DWI with iso-intensity on apparent diffusion coefficient (ADC) map.

• Pediatric Infection and Vaccine
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• v.30 no.3
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• pp.180-187
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• 2023

In Korea, >90% of children and adolescents aged <19 years have been infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) since 2020. Among confirmed cases of pediatric coronavirus disease 2019 (COVID-19), 40-60% of patients developed neurologic symptoms such as seizures, headache, and encephalitis. Herein, we report the case of a 3-year-old female patient with SARS-CoV-2 infection who presented with seizures and altered consciousness and was diagnosed with COVID-19 encephalitis. The patient recovered after treatment with intravenous immunoglobulin, high-dose steroids, anti-seizure drugs, and an anti-viral agent. She was discharged after regaining the ability to speak words and walk alone on hospital day 39. Complete recovery was observed at the 1-year follow-up. The findings in this case suggest that early detection and active intervention is associated with better outcomes in patients with COVID-19 encephalitis.

• Molecules and Cells
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• v.21 no.1
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• pp.112-120
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• 2006

It has been suggested that defective interfering (DI) RNA contributes to the persistence of Japanese encephalitis virus (JEV). In this study, we characterized molecular and biological aspects of the DI RNA and its relation to viral persistence. We identified a homologous DI virus intimately associated with JEV persistence in Vero cells. The production of DI RNA during undiluted serial passages of JEV coincided with the appearance of cells refractory to acute infection with JEV. We also established a Vero cell clone with a persistent JEV infection in which the DI RNA coreplicated efficiently at the expense of helper virus. The infectious virus yield of the clone fluctuated during its growth depending upon the amount of DI RNA accumulated in the previous replication cycle. Identification of the corresponding negative-sense RNA of the DI RNA indicated that the DI RNA functioned as a replication unit. Most of the DI RNA molecules retained their open reading frames despite a large deletion, encompassing most of the prM, the entire E, and the 5' half of the NS1 gene. Taken together, these observations suggest that the generation of homologous DI RNA during successive JEV acute infections in Vero cells probably participates actively in persistent JEV infection.

• Clinical and Experimental Pediatrics
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• v.54 no.6
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• pp.234-240
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• 2011

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease of the central nervous system (CNS) that typically presents as a monophasic disorder associated with multifocal neurologic symptoms and encephalopathy. ADEM is considered an autoimmune disorder that is triggered by an environmental stimulus in genetically susceptible individuals. The diagnosis of ADEM is based on clinical and radiological features. Most children with ADEM initially present with fever, meningeal signs, and acute encephalopathy. The level of consciousness ranges from lethargy to frank coma. Deep and subcortical white-matter lesions and gray-matter lesions such as thalami and basal ganglia on magnetic resonance imaging (MRI) are associated with ADEM. In a child who presents with signs of encephalitis, bacterial and viral meningitis or encephalitis must be ruled out. Sequential MRI is required to confirm the diagnosis of ADEM, as relapses with the appearance of new lesions on MRI may suggest either multiphasic ADEM or multiple sclerosis (MS). Pediatric MS, defined as onset of MS before the age of 16, is being increasingly recognized. MS is characterized by recurrent episodes of demyelination in the CNS separated in space and time. The McDonald criteria for diagnosis of MS include evidence from MRI and allow the clinician to make a diagnosis of clinically definite MS on the basis of the interval preceding the development of new white matter lesions, even in the absence of new clinical findings. The most important alternative diagnosis to MS is ADEM. At the initial presentation, the 2 disorders cannot be distinguished with certainty. Therefore, prolonged follow-up is needed to establish a diagnosis.

• Investigative Magnetic Resonance Imaging
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• v.19 no.3
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• pp.186-190
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• 2015

Acute disseminated encephalomyelitis (ADEM) is a demyelinating and inflammatory condition of the central nervous system, occurring predominantly in white matter. ADEM involving the rhombencephalon without affecting the white matter is very rare. Here, we present an unusual case of ADEM involving only the rhombencephalon in a 4-year-old Asian girl. The patient complained of pain in the right lower extremities, general weakness, ataxia, and dysarthria. The initial brain CT showed subtle ill-defined low-density lesions in the pons and medulla. On brain MRI, T2 high signal intensity (T2-HSI) lesions with mild swelling were present in the pons, both middle cerebellar peduncles, and the anterior medulla. The initial diagnosis was viral encephalitis involving the rhombencephalon. Curiously, a cerebrospinal fluid (CSF) study revealed no cellularity, and negative viral marker findings. Three weeks later, follow up brain MRI showed that the extent of the T2-HSI lesions in the brain stem had decreased. After reinvestigation, it was found that she had a prior history of upper respiratory infection. In this case, we report the very rare case of a patient showing isolated involvement of the rhombencephalon in ADEM, mimicking viral rhombencephalitis on CT and MR imaging. ADEM can involve unusual sites such as the rhombencephalon in isolation, without involvement of the white matter or deep gray matter and, therefore, should be considered even when it appears in unusual anatomical areas. Thorough history taking is important for making a correct diagnosis.

• Korean Journal of Veterinary Research
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• v.36 no.2
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• pp.405-415
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• 1996

This study was carried out to investigate the distribution of inclusion bodies in the tissues as well as to observe the general histopathological lesions of dogs infected with canine distemper. And also, the reliability of diagnostic values of inclusion bodies and the distribution of viral antigen in tissues were inspected by immunohistochemistry with monoclonal antibody. The results obtained were as follows; 1. Pneumonia observed in dogs infected with canine distemper virus was classified into interstitial, broncho-, and broncho-interstitial pneumonia histopathologically. Each occurring ratio was 35, 45 and 20%. 2. Histopathological classification of the canine distemper encephalitis was 20% in acute, 60% in subacute, and 20% in chronic encephalitis, respectively. 3. The organs in which inclusion bodies were predominantly distributed were stomach(82.6%), cerebellum(62.9%), lung(62.1%), cerebrum(50.0%), urinary bladder (46.1%), kidney(36.0%) and pancreas(25.0%). Intracytoplasmic inclusion bodies were mainly observed in the organs except the brain. 4. Canine distemper virus antigens were detected in the numerous tissues as well as in the inclusion bodies observed in the various organs. Antigen detection ratios in the lung, cerebellum and cerebrum were 68.9, 70.4 and 52.2%, respectively. These ratios were somewhat higher than those of inclusion bodies observed in the organs. 5. Canine distemper virus was mainly distributed in astrocytes and ependymal cells in the brain. These results suggested that the histopathologic diagnosis of canine distemper was reliable, and the spread of canine distemper virus in the brain was related with cerebrospinal fluid pathway.

• Journal of the Korean Society of Radiology
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• v.82 no.5
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• pp.1274-1280
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• 2021

Acute necrotizing encephalopathy (ANE) is a rare but distinctive type of influenza-associated encephalopathy characterized by symmetric multiple lesions with an invariable thalamic involvement. Although the exact pathogenesis of ANE remains unclear, the most prevalent hypothesis is the "cytokine storm," which results in blood-brain-barrier breakdown. We present the case of a 10-year-old boy with fulminant ANE confirmed with serial MRI studies, including diffusion-weighted imaging and susceptibility-weighted imaging. A comparison of these serial images demonstrated detailed and longitudinal changes in MRI findings during the clinical course corresponding to pathophysiological changes. Our case clarifies the pathogenesis of ANE brain lesions using serial imaging studies and suggests that early immunomodulatory therapy reduces brain damage.