ABSTRACT
Nipah virus infection is known to cause late-onset and relapsed encephalitis, in addition to an acute encephalitic illness. This is a report of a 35 years old woman, who had exposure to the Nipah virus infection during the 1999 Malaysian outbreak, was positive for Nipah IgG by immunofl uorescence, and had multiple small hyperintense lesions in brain MRI typically seen in acute Nipah encephalitis patients, indicating asymptomatic Nipah virus infection. She subsequently developed acute encephalitis after 11 years, manifesting as diplopia, internuclear opthalmoplegia and epileptic seizures with pleocytosis in cerebrospinal fl uid examination. She had another episode of relapsed encephalitis a year later, with seizures, memory impairment, chorea and new lesions in MRI brain. This patient is unusual in the long incubation of 11 years before manifesting with late-onset Nipah encephalitis.
ABSTRACT
Phylogenetic analysis of Nipah virus isolates from Malaysia, Bangladesh and Cambodia suggested the presence of at least two different clusters of NiV strains. Based on the major glycoprotein (G) gene, the Nipah virus-Tambun isolate clustered with Nipah virus isolates from Cambodia and Bangladesh, whereas the remaining isolates from Malaysia clustered in a separate cluster. Sequence heterogeneity among the Nipah virus isolates from Malaysia was noted but the overall genomic sequence divergence value was small, suggesting a possible recent introduction of the virus. Nipah virus replicated well in porcine stable kidney cells and human lung fibroblast cells. Human monocytes, on the other hand were infected with Nipah virus but the cells did not support productive infection. Similarly, infection of human neuronal cells did not result in release of high infectious virus yield. The monocytes can serve to disseminate Nipah virus from site of infection including across the blood-brain barrier. And in the brain, Nipah virus is probably spread through cell-to-cell spread mechanism.
ABSTRACT
At least three major antigenic dengue 2 virus proteins were recognized by pooled dengue fever patients' sera in infected Aedes albopictus (C6/36) mosquito cells. Dengue virus envelope (E), premembrane (PrM) and non-structural protein 1 (NS 1) dimer were detected beginning on day 3 postinfection in both the cell membrane and cytosolic fractions. Using the patients' sera, the presence of antigenic intermediate core protein (C)-PrM and NS1-non-structural protein 2a (NS2a) in the cytoplasmic fraction of dengue 2 virus infected cells was revealed. The presence of a approximately 92 and approximately 84 kDa NS 1 dimer in the membrane (NS 1m) and cytosolic (NS 1c) fractions of C6/36 cells, respectively, was also recognized. Using individual patient's serum, it was further confirmed that all patients' sera contained antibodies that specifically recognized E, NS 1 and PrM present in the dengue 2 virus-infected cell membrane fractions, suggesting that these glycosylated virus proteins were the main antigenic proteins recognized in vivo. Detection of dengue 2 virus C antibody in some patients further suggested that C could be antigenic if presented in vivo.