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Related Experiment Video

Updated: May 18, 2026

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
09:13

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy

Published on: November 1, 2011

Heparan sulfate facilitates Rift Valley fever virus entry into the cell.

S M de Boer1, J Kortekaas, C A M de Haan

  • 1Department of Infectious Diseases & Immunology, Virology Division, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.

Journal of Virology
|September 28, 2012
PubMed
Summary

Rift Valley fever virus (RVFV) requires heparan sulfate, a molecule on cell surfaces, for effective entry into host cells. This finding is crucial for understanding RVFV infection and developing antiviral strategies.

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Last Updated: May 18, 2026

Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
09:13

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Published on: November 1, 2011

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Highly Sensitive Assay for Measurement of Arenavirus-cell Attachment
08:34

Highly Sensitive Assay for Measurement of Arenavirus-cell Attachment

Published on: March 2, 2016

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Rift Valley fever virus (RVFV) is an emerging arthropod-borne pathogen with broad host and cell tropism.
  • Understanding the molecular mechanisms of RVFV entry is critical for controlling its spread.

Purpose of the Study:

  • To investigate the role of cell surface molecules in RVFV entry.
  • To identify specific host factors required for efficient RVFV infection.

Main Methods:

  • Virus neutralization assays using heparin.
  • Enzymatic removal of cell surface heparan sulfate.
  • Analysis of RVFV entry in genetically modified cells lacking heparan sulfate synthesis.

Main Results:

  • Heparan sulfate, a glycosaminoglycan, is essential for efficient RVFV entry.
  • Preincubation with heparin significantly reduced viral entry.
  • Enzymatic removal or genetic deficiency of heparan sulfate markedly impaired RVFV infection.

Conclusions:

  • Heparan sulfate acts as a key host cell receptor or co-receptor for RVFV.
  • Targeting heparan sulfate interactions could be a potential therapeutic strategy against RVFV.