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04:23
A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Lectin switching during dengue virus infection.
Wanwisa Dejnirattisai1, Andrew I Webb, Vera Chan
1Department of Medicine, Faculty of Medicine, Imperial College London, United Kingdom.
The Journal of Infectious Diseases
|May 25, 2011
Summary
Dengue virus interaction with dendritic cell receptors DC-SIGN and L-SIGN depends on virus origin. Virus from human cells, unlike insect cells, cannot bind DC-SIGN, impacting dengue infection studies.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Dengue virus receptors are not well understood.
- Dendritic cell-specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin (DC-SIGN) and liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN) bind dengue virus and enhance infection.
Purpose of the Study:
- To investigate the interaction of dengue viruses with DC-SIGN and L-SIGN.
- To determine how virus production in different cell types affects this interaction.
Main Methods:
- Produced dengue viruses in insect cells, tumor cell lines, and primary human dendritic cells (DCs).
- Studied the binding and infectivity of these viruses with DC-SIGN and L-SIGN expressing cells.
Main Results:
- Dengue virus produced in primary DCs did not interact with DC-SIGN but remained infectious for L-SIGN-expressing cells.
- Virus glycosylation, dependent on cell state, influences interaction with DC-SIGN and L-SIGN.
Conclusions:
- Skin-resident DCs might be an initial site for insect-produced dengue virus infection.
- Dendritic cells are unlikely to support large-scale dengue virus replication.
- Caution is advised when interpreting dengue virus tropism studies using viruses from insect cells or tumor lines due to differential glycosylation.
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