Detection of dengue virus by in situ hybridization

Killen, Helen M.; O’Sullivan, Matthew L.

doi:10.1016/0166-0934(93)90121-7

Cited by 36 publications

(29 citation statements)

References 27 publications

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“…The endothelial cell line ECV304, derived from human umbilical cord was identified to be susceptible to DEN-2 infection and was used to study the molecular mechanism of DEN-2 binding to endothelial cells (Bonner and O' Sullivan, 1998;Killen and O' Sullivan, 1993). When VOPBA was employed, it was found that DEN-2 binds to three membrane proteins (29, 34 and 43 KD.a respectively), of ECV304 cells (Wei eta/., 2003).…”

Section: -103mentioning

confidence: 99%

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

Seema

Jain

2005

Indian J Clin Biochem

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Dengue fever is one of the major health problems in India. Interaction with specific receptor(s) at the cell surface is one of the first events in the pathogenesis of Dengue virus. However, relatively little is known about these receptors. Cellular receptors in human monocytes and mouse neural cells are main target for the viral infection. The envelope protein of the virus (E-protein) plays important role in attachment of virus to target cells and their interaction with cellular receptors. The modulation of receptor gene(s) and/or protein(s) can be used as a method for interfering with virus entry and can thus become a new method for disease prevention. The receptors can be purified by affinity chromatography using E-protein as ligand. It has been reported that addition of highly sulfated heparan sulfate prevents E-protein binding to target cells suggesting that heparan sulfate is utilized by dengue envelope protein to bind to target cells.

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Section: -103mentioning

confidence: 99%

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

Seema

Jain

2005

Indian J Clin Biochem

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“…16 Briefly, dewaxed tissue sections were pretreated with HCl followed by 0.1 mg/ml of proteinase K in 100 mmol/L Tris/50 mmol/L ethylenediaminetetraacetic acid, pH 8.0 buffer (15 minutes, 37°C), followed by two PBS washes. Washes with glycine and prehydridization steps were omitted.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

A Golden Hamster Model for Human Acute Nipah Virus Infection

Wong

Grosjean

Brisson

et al. 2003

The American Journal of Pathology

210

229

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A predominantly pig-to-human zoonotic infection caused by the novel Nipah virus emerged recently to cause severe morbidity and mortality in both animals and man. Human autopsy studies showed the pathogenesis to be related to systemic vasculitis that led to widespread thrombotic occlusion and microinfarction in most major organs especially in the central nervous system. There was also evidence of extravascular parenchymal infection, particularly near damaged vessels A recent outbreak of a novel paramyxovirus subsequently named Nipah virus (NiV) infected hundreds of patients in Malaysia causing severe morbidity and a mortality rate of ϳ40%.

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“…Nevertheless, an increasing number of reports have indicate that DV can infect human endothelial cells as well. [13][14][15][16] In addition, chimeric DV envelope protein has been shown to bind to endothelial cells, indicating the endothelium can be a target for DV infection. 17 However, the results of these studies are questionable because many used a human endothelial cell line (ECV 304) that is a derivative of human bladder cell line T24 from the American Type Culture Collection.…”

Section: Ribavirin Inhibits Dv-induced Il-6 and Il-8 Production By Humentioning

confidence: 99%

Dengue virus infects human endothelial cells and induces IL-6 and IL-8 production.

Huang¹,

Lei²,

Liu³

et al. 2000

The American Journal of Tropical Medicine and Hygiene

158

148

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Abstract. In this study dengue virus (DV) was found to infect primary endothelial cells derived from human umbilical cord veins (HUVEC) and alter their cytokine production. Dengue virus infection of HUVEC was confirmed by an increase in plaque-forming units in the culture supernatant and by immunofluorescence assay. HUVEC produced large amounts of interleukin (IL)-6 and IL-8 but not IL-1␤ after DV infection. Both the replication of DV and the production of IL-6 and IL-8 by HUVEC after DV infection were inhibited by ribavirin, an antiviral synthetic guanosine analogue. Additionally, increased serum levels of IL-6 and IL-8 were observed in patients with dengue hemorrhagic fever but not dengue fever. Therefore, our results suggest that endothelial cells can be a target for DV infection, and that DV-induced IL-6 and IL-8 production by endothelial cells may contribute to the pathogenesis of dengue hemorrhagic fever.

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Detection of dengue virus by in situ hybridization

Cited by 36 publications

References 27 publications

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

Molecular mechanism of pathogenesis of dengue virus: Entry and fusion with target cell

A Golden Hamster Model for Human Acute Nipah Virus Infection

Dengue virus infects human endothelial cells and induces IL-6 and IL-8 production.

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