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High-throughput Screening for Small-molecule Modulators of Inward Rectifier Potassium Channels

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Published on: January 27, 2013

Modulation of Potassium Channels Inhibits Bunyavirus Infection.

Samantha Hover¹, Barnabas King², Bradley Hall¹

¹From the School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT.

The Journal of Biological Chemistry

|December 18, 2015

Summary

This summary is machine-generated.

Bunyamwera virus requires cellular potassium channels for infection, crucial for early viral entry. This discovery suggests potassium channel modulators could offer new treatments for bunyavirus diseases.

Keywords:

antiviral agent ion channel negative-strand RNA virus pathogenesis potassium channel

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MicroRNA-based Regulation of Picornavirus Tropism

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Published on: February 6, 2017

Area of Science:

Virology
Molecular Biology
Pathogen Discovery

Background:

Bunyaviruses are significant emerging pathogens with global health and economic impact.
The segmented genome of bunyaviruses facilitates reassortment, leading to novel strains with altered pathogenicity.
Current treatments for human bunyavirus infections are lacking, necessitating the urgent development of new antiviral strategies.

Purpose of the Study:

To investigate the cellular mechanisms underlying bunyavirus infection.
To identify host factors essential for Bunyamwera virus (BUNV) entry and replication.
To explore potential therapeutic targets for bunyavirus infections.

Main Methods:

Utilized time-of-addition assays with potassium (K+) channel modulators to determine critical infection stages.
Screened K+ channel modulators to identify specific channel families involved in BUNV infection.
Tested K+ channel dependence in other bunyaviruses, including Schmallenberg virus and Hazara virus.

Main Results:

Bunyamwera virus (BUNV) activates and requires cellular potassium (K+) channels for cell entry.
K+ channel function is essential shortly after virus entry and before viral RNA synthesis.
A similar K+ channel dependence was observed for Schmallenberg virus and Hazara virus.
Two-pore domain K+ channels (K2P) were identified as the key mediators of BUNV K+ channel dependence.

Conclusions:

Cellular potassium channels are critical host factors for bunyavirus infection.
Two-pore domain K+ channels (K2P) represent a novel therapeutic target for bunyavirus diseases.
Existing K2P channel modulators, some in clinical use, may offer a new class of safe antiviral drugs for treating lethal bunyavirus infections.