Role of c-ABL in DENV-2 Infection and Actin Remodeling in Vero Cells

TL;DR

This study shows that the c-ABL protein is important for Dengue virus infection and changes in cell structure, suggesting it could be a target for antiviral treatments.

Contribution

The study identifies c-ABL as a host factor involved in DENV infection and cytoskeletal changes, proposing it as a potential antiviral target.

Findings

c-ABL is necessary for DENV entry and envelope protein accumulation in infected cells.

Inhibiting c-ABL reduces F-actin reorganization caused by DENV infection.

c-ABL is linked to endothelial dysfunction in DENV infection and host secreted factors.

Abstract

In this study, we address the role of c-ABL (cellular Abelson Tyr kinase) in the cytoskeletal rearrangements induced by DENV (Dengue virus) infection in mammalian cells. Using the specific inhibitor imatinib and targeted RNA interference, we show that c-ABL is necessary for viral entry and subsequent ENV (DENV envelope protein) accumulation in infected cells. In addition, c-ABL targeting attenuates F-actin reorganization induced by DENV infection. Together with the involvement of c-ABL in endothelial dysfunction induced by DENV and host secreted factors, our findings strongly suggest that c-ABL is a potential host-targeted antiviral that could control DENV infection and/or its evolution to more severe forms of the disease.

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