Investigating the role of chloride channels during the Bunyamwera virus lifecycle.

Abstract

Bunyamwera virus (BUNV) is a mosquito-borne human pathogen that belongs to the Peribunyavirus family of the order Bunyavirales and is the prototypic Orthobunyavirus. Bunyaviruses can be transmitted by a variety of arthropod vectors and rodents and have established a global disease pattern that threatens human health, animal welfare, and food security. No vaccines or anti-viral therapies for any bunyavirus members are currently available. Given the emergence of this virus family into new geographical regions, their disease prevalence is increasing, and new anti-viral strategies are urgently required. Ion channels represent druggable host factors that can impede virus infections at a range of lifecycle stages. In this study, it was shown that BUNV requires cellular chloride (Cl− ) channels to establish an infection, as broad-spectrum Cl− channel blockers could impede virus infection in cultured cells. Using a defined panel of pharmacological tools to block specific Cl− family members, specific Cl− channel targets were identified as required by BUNV. This reveals the potential of Cl− channel modulating compounds as new and much needed anti-BUNV agents.