# SNX11 Deletion Inhibits Dabie bandavirus Infection by Interfering with the Assembly of V-ATPase

## TL;DR

SNX11 deletion stops Dabie bandavirus and other viruses by disrupting the V-ATPase assembly, which affects endosomal pH and viral release.

## Contribution

SNX11's role in V-ATPase assembly and its broad antiviral potential are newly identified.

## Key findings

- SNX11 interacts with the V1 subunit of V-ATPase, affecting its expression on endosomal membranes.
- SNX11 deletion inhibits replication of dengue, hantavirus, and influenza viruses.
- Altered endosomal pH due to SNX11 loss may hinder viral release into the cytoplasm.

## Abstract

SNX11, a sorting nexin protein localized on the endosomal membrane, is an important protein closely related to protein sorting and endosomal trafficking. Previously, through a genome-wide CRISPR screening, we identified SNX11 as a critical protein for the entry of Dabie bandavirus. SNX11 deletion significantly inhibits the replication of Dabie bandavirus. We further discovered that the loss of SNX11 alters endosomal pH, potentially affecting the release process of Dabie bandavirus from endosomes to the cytoplasm. However, the mechanism by which SNX11 modulates endosomal pH and whether SNX11 deletion similarly inhibits other viruses remain to be elucidated. This study reveals that SNX11 can interact with the V1 subunit of the endosomal proton pump V-ATPase, affecting the expression level of this subunit on the endosomal membrane and thereby disrupting the assembly of V-ATPase. Additionally, we found that SNX11 deletion significantly inhibits the replication of dengue virus, hantavirus, and influenza virus. These findings suggest that SNX11 may be a key protein in the process of viral infection and could serve as a broad-spectrum antiviral target.