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

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Bta-miR-101 suppresses BEFV replication via targeting NKRF.

Wendong Zhao¹, Peili Hou¹, Wenqing Ma¹

¹Ruminant Disease Research Center, College of Life Science, Shandong Normal University, Shandong Province, China.

Veterinary Microbiology

|May 31, 2021

Summary

Bovine transient fever virus (BEFV) infection is regulated by bta-miR-101, a microRNA that inhibits viral replication. This microRNA targets NF-κB repressing factor (NKRF), reducing apoptosis and viral load.

Keywords:

Apoptosis Bovine ephemeral fever virus (BEFV)Bta-miR-101 NF-κB-repressing factor (NKRF)Viral replication

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Area of Science:

Virology
Molecular Biology
Immunology

Background:

MicroRNAs (miRNAs) are small noncoding RNAs regulating gene expression.
Cellular miRNA roles in bovine transient fever virus (BEFV) infection are not well understood.
Investigating host-pathogen interactions in bovine viral diseases.

Purpose of the Study:

To elucidate the role and mechanism of cellular miRNAs in BEFV infection.
To identify specific miRNAs involved in the host response to BEFV.
To explore potential antiviral strategies based on miRNA regulation.

Main Methods:

Madin-Darby Bovine Kidney (MDBK) cell culture and BEFV infection model.
Quantitative real-time PCR to measure miRNA and gene expression.
Dual luciferase reporter assay to confirm miRNA-target interaction.
Apoptosis assays and viral replication quantification.

Main Results:

Bta-miR-101 expression was significantly upregulated in BEFV-infected MDBK cells.
Overexpression of bta-miR-101 inhibited BEFV replication, while inhibition of bta-miR-101 enhanced it.
NF-κB repressing factor (NKRF) was identified as a direct target of bta-miR-101.
NKRF promotes BEFV replication and induces apoptosis; bta-miR-101 suppresses this effect.

Conclusions:

Bta-miR-101 acts as an antiviral host factor against BEFV infection.
Bta-miR-101 inhibits BEFV replication by targeting NKRF and suppressing apoptosis.
This study reveals a novel antiviral mechanism and provides a basis for BEFV therapeutic strategies.