Sorafenib Impedes Rift Valley Fever Virus Egress by Inhibiting Valosin-Containing Protein Function in the Cellular Secretory Pathway

Abstract

There is an urgent need for therapeutic development to combat infections caused by Rift Valley fever virus (RVFV), which causes devastating disease in both humans and animals. In an effort to repurpose drugs for RVFV treatment, our previous studies screened a library of FDA-approved drugs. The most promising candidate identified was the hepatocellular and renal cell carcinoma drug sorafenib. Mechanism-of-action studies indicated that sorafenib targeted a late stage in virus infection and caused a buildup of virions within cells. In addition, small interfering RNA (siRNA) knockdown studies suggested that nonclassical targets of sorafenib are important for the propagation of RVFV. Here we extend our previous findings to identify the mechanism by which sorafenib inhibits the release of RVFV virions from the cell. Confocal microscopy imaging revealed that glycoprotein Gn colocalizes and accumulates within the endoplasmic reticulum (ER) and the transport of Gn from the Golgi complex to the host cell membrane is reduced. Transmission electron microscopy demonstrated that sorafenib caused virions to be present inside large vacuoles inside the cells. p97/valosin-containing protein (VCP), which is involved in membrane remodeling in the secretory pathway and a known target of sorafenib, was found to be important for RVFV egress. Knockdown of VCP resulted in decreased RVFV replication, reduced Gn Golgi complex localization, and increased Gn ER accumulation. The intracellular accumulation of RVFV virions was also observed in cells transfected with siRNA targeting VCP. Collectively, these data indicate that sorafenib causes a disruption in viral egress by targeting VCP and the secretory pathway, resulting in a buildup of virions within dilated ER vesicles.

Document Details

Document Type
Pub Defense Publication
Publication Date
Nov 01, 2017
Source ID
10.1128/jvi.00968-17

Entities

People

  • Ashwini Brahms
  • Chelsea L Pinkham
  • Farooq Nasar
  • Krishna Kota
  • Kylene Kehn-Hall
  • Rajini Mudhasani
  • Rouzbeh Zamani
  • Sina Bavari

Organizations

  • Defense Threat Reduction Agency
  • George Mason University
  • United States Army Medical Research Institute of Infectious Diseases
  • United States Department of Homeland Security
  • University of Nebraska Medical Center

Tags

Fields of Study

  • Biology

Readers

  • Infectious Disease/Epidemiology
  • Molecular and Cellular Biochemistry
  • Oncology

Technology Areas

  • Microelectronics