Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep40923
Title: Dengue virus compartmentalization during antibody-enhanced infection
Authors: Ong, E.Z
Zhang, S.L 
Tan, H.C 
Gan, E.S 
Chan, K.R 
Ooi, E.E 
Keywords: leukocyte antigen
leukocyte immunoglobulin like receptor subfamily B member 1
LILRB1 protein, human
protein tyrosine phosphatase SHP 1
PTPN6 protein, human
antibody dependent enhancement
dengue
Dengue virus
human
immunology
metabolism
phagosome
physiology
tumor cell line
virus entry
Antibody-Dependent Enhancement
Antigens, CD
Cell Line, Tumor
Dengue
Dengue Virus
Humans
Leukocyte Immunoglobulin-like Receptor B1
Phagosomes
Protein Tyrosine Phosphatase, Non-Receptor Type 6
Virus Internalization
Issue Date: 2017
Citation: Ong, E.Z, Zhang, S.L, Tan, H.C, Gan, E.S, Chan, K.R, Ooi, E.E (2017). Dengue virus compartmentalization during antibody-enhanced infection. Scientific Reports 7 : 40923. ScholarBank@NUS Repository. https://doi.org/10.1038/srep40923
Abstract: Secondary infection with a heterologous dengue virus (DENV) serotype increases the risk of severe dengue, through a process termed antibody-dependent enhancement (ADE). During ADE, DENV is opsonized with non- or sub-neutralizing antibody levels that augment entry into monocytes and dendritic cells through Fc-gamma receptors (Fc3Rs). We previously reported that co-ligation of leukocyte immunoglobulin-like receptor-B1 (LILRB1) by antibody-opsonized DENV led to recruitment of SH2 domain-containing phosphatase-1 (SHP-1) to dephosphorylate spleen tyrosine kinase (Syk) and reduce interferon stimulated gene induction. Here, we show that LILRB1 also signals through SHP-1 to attenuate the otherwise rapid acidification for lysosomal enzyme activation following Fc 3R-mediated uptake of DENV. Reduced or slower trafficking of antibody-opsonized DENV to lytic phagolysosomal compartments, demonstrates how co-ligation of LILRB1 also permits DENV to overcome a cell-autonomous immune response, enhancing intracellular survival of DENV. Our findings provide insights on how antiviral drugs that modify phagosome acidification should be used for viruses such as DENV. © The Author(s) 2017.
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/173949
ISSN: 20452322
DOI: 10.1038/srep40923
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