Identification of dengue virus binding proteins using affinity chromatography

Upanan, Supranee; Kuadkitkan, Atichat; Smith, Duncan R.

doi:10.1016/j.jviromet.2008.05.001

Cited by 36 publications

(27 citation statements)

References 29 publications

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“…Interactions between GRP78 and dengue E protein have been proposed to occur at several steps of the cell cycle, and both cell surface and intracellular interactions between GRP78 and dengue E protein have been documented [24–26]. …”

Section: Discussionmentioning

confidence: 99%

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Voltage Dependent Anion Channel Is Redistributed during Japanese Encephalitis Virus Infection of Insect Cells

Fongsaran

Phaonakrop

Roytrakul

et al. 2014

The Scientific World Journal

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Despite the availability of an effective vaccine, Japanese encephalitis remains a significant cause of morbidity and mortality in many parts of Asia. Japanese encephalitis is caused by the Japanese encephalitis virus (JEV), a mosquito transmitted flavivirus. Many of the details of the virus replication cycle in mosquito cells remain unknown. This study sought to determine whether GRP78, a well-characterized flavivirus E protein interacting protein, interacted with JEV E protein in insect cells, and whether this interaction was mediated at the cell surface. GRP78 was shown to interact with JEV E protein by coimmunoprecipitation, and was additionally shown to interact with voltage dependent anion protein (VDAC) through the same methodology. Antibody inhibition experiments showed that neither GRP78 nor VDAC played a role in JEV internalization to insect cells. Interestingly, VDAC was shown to be significantly relocalized in response to JEV infection, and significant levels of colocalization between VDAC and GRP78 and VDAC and ribosomal L28 protein were seen in JEV infected but not uninfected cells. This is the first report of relocalization of VDAC in response to JEV infection and suggests that this may be a part of the JEV replication strategy in insect cells.

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Section: Discussionmentioning

confidence: 99%

“…GRP78 is a multifunctional chaperone protein that has been shown to interact with dengue virus E protein in a number of studies [24–26]. GRP78 is predominantly localized to the endoplasmic reticulum (ER) where it regulates the activation of the unfolded protein response (UPR) in response to stress conditions [27–29].…”

Section: Introductionmentioning

confidence: 99%

Voltage Dependent Anion Channel Is Redistributed during Japanese Encephalitis Virus Infection of Insect Cells

Fongsaran

Phaonakrop

Roytrakul

et al. 2014

The Scientific World Journal

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“…Recently, it has been reported that glucose-regulated protein 78 (GRP78), which resides principally within the ER, interacts with domain III of DENV E protein [56] . Knockdown of this protein reduces the production of infectious DENV particles [57] , suggesting an important role of this chaperone in the correct folding of DENV proteins.…”

Section: Discussionmentioning

confidence: 99%

Statins Reduce Dengue Virus Production via Decreased Virion Assembly

2011

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Background: Most of the effects of statins can be explained by pleiotropic effects independent of their lowering of serum cholesterol; in some cases, these effects have been shown to be a result of the role of statins in the prenylation of cellular proteins, some of which are involved in the life cycle of animal viruses. This study evaluated the potential antiviral activity of lovastatin (LOV) against dengue virus (DENV) infection of epithelial and endothelial cells (VERO cells, epithelial cells derived from African green monkey kidney, and HMEC-1 cells, human dermal microvascular endothelial cells). Methods: To evaluate its potential antiviral effects, LOV was used before, during and after inoculation of cell cultures with DENV. Results: Before and after viral inoculation, LOV caused a reduction in virus yield (80% for HMECs and 25% for VERO cells). However, with LOV treatment after inoculation induced a marked increase (2- to 9-fold) in viral-positive RNA while the amount of viral protein increased only by 13–23%. A moderate reduction (1 log unit) in viral titer occurred concurrent with the increase in DENV genomic RNA and protein within the cells. Conclusions: According to our results, LOV appears to have a greater effect on viral assembly than on replication, resulting in the cellular presence of viral genomic RNA and proteins that fail to take the normal assembly pathway.

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“…Interestingly, although usually an intracellular protein, GRP78 can also be localized on cell surface and the incubation of the hepatic cell lineage HepG2 with antibodies anti-GRP78 reduced cell infection by DENV-2 (Jindadamrongwech, Thepparit and Smith 2004;Upanan, Kuadkitkan and Smith 2008). These authors also studied DENV-1 binding to HepG2 cells.…”

Section: Putative Receptors and Attachment Factors In Mammalian Cellsmentioning

confidence: 99%

Receptors and routes of dengue virus entry into the host cells

Cruz-Oliveira

Freire

Conceição

et al. 2015

FEMS Microbiology Reviews

258

211

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One-sentence summary: This review addresses the structural rearrangements of dengue virus proteins and their functions during virus entry into the host cells, exploring (a) the cellular elements involved in virus binding to mammalian and mosquito cells, (b) the internalization routes that ultimately lead to virus entry into the cell and (c) the mechanisms by which viral genome gain access to the cytoplasm, including original insights from our recent work that supports the hypothesis that the capsid protein has a role in this process. Editor: Urs Greber ABSTRACTDengue is the most prevalent arthropod-borne viral disease, caused by dengue virus, a member of the Flaviviridae family. Its worldwide incidence is now a major health problem, with 2.5 billion people living in risk areas. In this review, we integrate the structural rearrangements of each viral protein and their functions in all the steps of virus entry into the host cells. We describe in detail the putative receptors and attachment factors in mammalian and mosquito cells, and the recognition of viral immunocomplexes via Fcγ receptor in immune cells. We also discuss that virus internalization might occur through distinct entry pathways, including clathrin-mediated or non-classical clathrin-independent endocytosis, depending on the host cell and virus serotype or strain. The implications of viral maturation in virus entry are also explored. Finally, we discuss the mechanisms of viral genome access to the cytoplasm. This includes the role of low pH-induced conformational changes in the envelope protein that mediate membrane fusion, and original insights raised by our recent work that supports the hypothesis that capsid protein would also be an active player in this process, acting on viral genome translocation into the cytoplasm.

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Identification of dengue virus binding proteins using affinity chromatography

Cited by 36 publications

References 29 publications

Voltage Dependent Anion Channel Is Redistributed during Japanese Encephalitis Virus Infection of Insect Cells

Voltage Dependent Anion Channel Is Redistributed during Japanese Encephalitis Virus Infection of Insect Cells

Statins Reduce Dengue Virus Production via Decreased Virion Assembly

Receptors and routes of dengue virus entry into the host cells

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