Background And Purpose: Japanese encephalitis virus infection is a sporadic infectious disease in Taiwan. Despite progress in laboratory examinations and imaging studies, diagnosis of Japanese encephalitis remains underestimated. This study was conducted to identify clinical symptoms and laboratory findings that may assist in early identification of this disease.
Methods: This retrospective study included all patients diagnosed with Japanese encephalitis at Kaohsiung Veterans General Hospital from January 2000 through December 2007. Epidemiologic data, predisposing factors, neurological and non-neurological signs and symptoms, laboratory data, and treatment were analyzed. Outcomes and neurological complications were evaluated.
Results: Eleven patients had Japanese encephalitis, and 10 had sufficient information for enrolment into the study. Nine patients presented with non-significant constitutional symptoms of fever, nausea, or headache. Other signs and symptoms included rhinorrhea, sore throat, abdominal pain, cough, myalgia, or arthralgia. Eight patients had lymphocytic pleocytosis with elevated protein and borderline low glucose levels in the cerebrospinal fluid. Leptomeningeal enhancement and low density lesions were the most common computed tomography findings. T2 hyperintensity lesions and leptomeningeal enhancement were seen in 5 patients. Two patients presenting with acute flaccid paralysis had high intensity lesions on the thalamus and basal ganglion. There were no correlations between clinical, laboratory, and imaging findings. None of the patients had neurological sequelae.
Conclusions: Presentations, laboratory examination, and clinical signs are not specific for Japanese encephalitis. Sporadic cases are usually seen from May to August, which are associated with monsoon rains. Hence increased awareness of this disease is recommended during these periods.
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Japanese encephalitis (JE) is a mosquito-borne infectious disease caused by the Japanese encephalitis virus (JEV). There is currently no effective treatment for JE, and all approved Japanese encephalitis vaccine products originated from the JEV genotype III (GIII). In recent years, JEV genotype I (GI) has gradually replaced GIII as the dominant genotype, and a new symptom of peripheral nerve injury (PNI) caused by JEV NX1889 strain has attracted wide attention, in which JEV envelope (E) protein may be involved in early peripheral nerve injury.
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Department of Animal Dairy and Veterinary Sciences, College of Agriculture and Applied Sciences, Utah State University, Logan, UT 84322, USA.
Zika virus (ZIKV) is a medically important mosquito-borne orthoflavivirus, but no vaccines are currently available to prevent ZIKV-associated disease. In this study, we compared three recombinant chimeric viruses developed as candidate vaccine prototypes (rJEV/ZIKV, rJEV/ZIKV, and rJEV/ZIKV), in which the two neutralizing antibody-inducing prM and E genes from each of three genetically distinct ZIKV strains were used to replace the corresponding genes of the clinically proven live-attenuated Japanese encephalitis virus vaccine SA-14-2 (rJEV). In WHO-certified Vero cells (a cell line suitable for vaccine production), rJEV/ZIKV exhibited the slowest viral growth, formed the smallest plaques, and displayed a unique protein expression profile with the highest ratio of prM to cleaved M when compared to the other two chimeric viruses, rJEV/ZIKV and rJEV/ZIKV, as well as their vector, rJEV.
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