Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Abstract

Background: Rift Valley fever virus is a single-stranded RNA virus that causes disease in humans and livestock. Results: Rift Valley fever virus infection activates the host NFB signaling cascade. Conclusion: NFB inhibitors, particularly curcumin, down-regulate virus in both in vitro and in vivo models. Significance: Novel versions of host components resulting from an infection make them ideal therapeutic targets.

Venezuelan equine encephalitis virus non-structural protein 3 (nsP3) interacts with RNA helicases DDX1 and DDX3 in infected cells

“…A 30% slurry of Protein AþG beads was added to the immunoprecipitates and incubated for 2 h with rotation at 4 C. The immunoprecipitates were centrifuged briefly at 4 C for 2 min at 2000 rpm and beads were washed 3Â with TNE50 þ 0.1% NP-40. LC-MS/MS analysis was carried out as previously described (Amaya et al, 2014;Narayanan et al, 2012).…”

Small molecule inhibitors of Ago2 decrease Venezuelan equine encephalitis virus replication

“…Immobilization and staining were performed as described in Narayanan et al (2012) for neutral red staining, or Kehn-Hall et al (2012) for crystal violet staining. Plaques were assessed at two days post infection.…”

Characterizing the effect of Bortezomib on Rift Valley Fever Virus multiplication

“…In order to evaluate the therapeutic potential of Bortezomib for the treatment of RVFV infections, we first determined its toxicity in HSAECs, a cell line that has been demonstrated to be a useful model for the study of RVFV infections Narayanan et al, 2012Narayanan et al, , 2011Popova et al, 2010). HSAECs were treated with 0.01 or 0.1 lM, concentrations of Bortezomib for 24 h after which survival was measured using the CellTiter Glo assay.…”

“…NSs is a critical virulence factor that is important for establishing a productive infection Bird et al, 2008;Habjan et al, 2009;Ikegami et al, 2009a;Le May et al, 2008;Narayanan et al, 2012;Vialat et al, 2000). We hypothesized that the inhibitory potential of Bortezomib may, in part, involve an interference with known NSs-dependent phenomena in MP-12 infected cells.…”

“…There are no FDA-approved therapies to treat RVFV infection; however, recent research has indicated the importance of host factors to RVFV multiplication and provided proof of concept evidence of the efficacy of host-based inhibitors against RVFV infections Narayanan et al, 2012;Nuss et al, 2014;Popova et al, 2010). Bortezomib is an FDA-approved inhibitor of the 26S subunit of the proteasome, which has shown antiviral activity against multiple viruses (Adams and Kauffman, 2004;Bandi et al, 2010;Dudek et al, 2010;Raaben et al, 2010;Teale et al, 2009;Wang et al, 2010).…”