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Related Experiment Video

Updated: Apr 13, 2026

Measuring Dengue Virus RNA in the Culture Supernatant of Infected Cells by Real-time Quantitative Polymerase Chain Reaction
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Measuring Dengue Virus RNA in the Culture Supernatant of Infected Cells by Real-time Quantitative Polymerase Chain Reaction

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Dengue virus binding and replication by platelets.

Ayo Y Simon1, Michael R Sutherland1, Edward L G Pryzdial1

  • 1Canadian Blood Services, Centre for Innovation, Ottawa, ON, Canada; and Centre for Blood Research/Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.

Blood
|May 7, 2015
PubMed
Summary
This summary is machine-generated.

Platelets bind Dengue virus (DENV) and replicate its genome, producing infectious virus. This finding offers new insights into DENV-induced thrombocytopenia and potential viral replication by platelets.

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A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
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Area of Science:

  • Virology
  • Immunology
  • Hematology

Background:

  • Dengue virus (DENV) causes severe illness, with thrombocytopenia being a common but poorly understood feature.
  • Mechanisms of platelet reduction during DENV infection require further elucidation.

Purpose of the Study:

  • To investigate the direct interaction between DENV and platelets.
  • To determine if platelets can support DENV replication and progeny production.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction and antigen testing to confirm DENV-platelet binding.
  • Investigating coreceptors (DC-SIGN, heparan sulfate proteoglycan) using specific inhibitors.
  • Monitoring DENV genome replication and NS1 protein production in platelets over time.
  • Assessing viral infectivity and progeny generation in the presence of platelets.

Main Results:

  • Platelets exhibit saturable binding of DENV, with approximately 800 viruses binding per platelet at 37°C.
  • Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) and heparan sulfate proteoglycan are implicated as coreceptors.
  • Platelets actively replicate the DENV RNA genome, increasing viral load up to fourfold over seven days.
  • Platelets produce infectious DENV, moderating the intrinsic decay of viral infectivity and generating viable progeny.

Conclusions:

  • Platelets directly bind DENV and serve as a platform for its replication, producing infectious virus.
  • DENV antigen expression by platelets is a novel factor in DENV-induced thrombocytopenia.
  • Platelets may have the capacity to support the replication of other permissive RNA viruses.