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Related Experiment Video

Updated: Jun 12, 2026

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

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

Identification of Host Factors for Rift Valley Fever Phlebovirus.

Velmurugan Balaraman¹, Sabarish V Indran¹, Yonghai Li¹

¹Center of Excellence for Emerging and Zoonotic Animal Diseases, Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, 1800 Denison Ave, Manhattan, KS 66506, USA.

|November 25, 2023

Summary

Researchers identified WDR7 as a crucial host factor for Rift Valley fever phlebovirus (RVFV) replication. This finding is vital for developing new antiviral strategies against RVF and related bunyaviruses.

Keywords:

A549 cells LACV MP-12 RVFV WDR7 gene bunyavirus host factor phlebovirus

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Last Updated: Jun 12, 2026

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Published on: September 14, 2021

Area of Science:

Virology
Molecular Biology
Host-Pathogen Interactions

Background:

Rift Valley fever phlebovirus (RVFV) causes Rift Valley fever (RVF), a significant zoonotic disease with no current human vaccines or antivirals.
Understanding host factors influencing RVFV susceptibility and replication is critical for developing effective control strategies.
Previous research has not fully elucidated the host genes essential for RVFV infection and replication.

Purpose of the Study:

To identify host genes essential for Rift Valley fever phlebovirus (RVFV) replication using a large-scale genetic screen.
To validate the role of candidate host factors in RVFV replication and characterize their impact on the viral life cycle.
To investigate the function of WDR7 as a host factor for RVFV and La Crosse encephalitis virus (LACV) replication.

Main Methods:

Conducted CRISPR-Cas9 knockout screening in human A549 cells to identify host genes involved in RVFV replication.
Validated candidate genes using siRNA-mediated knockdowns and CRISPR-Cas9-mediated knockouts.
Assessed viral replication by measuring intracellular viral RNA accumulation and determining virus titers via plaque or TCID50 assays.

Main Results:

Identified approximately 900 genes potentially involved in RVFV infection and replication.
Silencing of WDR7 and LRP1 significantly impaired RVFV replication.
WDR7 knockout cells demonstrated significant effects on both intracellular RVFV RNA levels and viral titers, impacting RVFV replication later in its cycle (24h) and LACV earlier (12h).

Conclusions:

WDR7 is identified as an essential host factor required for the replication of both RVFV and LACV, viruses within the Bunyavirales order.
The findings highlight WDR7's critical role in facilitating phlebovirus replication, suggesting it as a potential target for antiviral therapies.
Further mechanistic studies are warranted to elucidate the precise role of WDR7 in the viral replication cycle.