Upregulation of the suppressors of cytokine signaling 1 and 3 is associated with arrest of phosphorylated-STAT1 nuclear importation and reduced innate response in denguevirus-infected macrophages

Tania Estrada-Jiménez, Lourdes Millán-Pérez Peña, Lilian Flores-Mendoza, Virginia Sedeño-Monge, Gerardo Santos-López, Nora Rosas-Murrieta, Sandra Reyes-Carmona, Eli Terán-Cabanillas, Jesus Hernández, Irma Herrera-Camacho, Verónica Vallejo-Ruiz, Julio Reyes-Leyva

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

© Mary Ann Liebert, Inc. 2016. To clarify whether the suppressors of cytokine signaling (SOCS) are associated with denguevirus (DENV) evasion of the antiviral response, we analyzed the expression kinetics of SOCS1 and SOCS3 and of the antiviral genes MxA and OAS during DENV infection of U937 macrophages that were or not treated with interferon (IFN)-α. DENV infection produced a viral titer three times higher in untreated than in IFN-α-treated cells (p < 0.001 at 72 h postinfection [p.i.]). Partial inhibition of DENV replication was associated with reduced expression of MxA and OAS antiviral genes as well as higher SOCS1 and SOCS3 expression in DENV-infected cells than in cells treated only with IFN-α. Complete loss of phosphorylated-signal transducer and activator of transcription (p-STAT)2 and reduced nuclear importation of p-STAT1 were observed in DENV-infected cells compared to IFN-α treatment that induced p-STAT1 and p-STAT2. Our data thus suggest that overexpression of SOCS1 and SOCS3 induced by DENV infection leads to impairment of antiviral response through the inhibition of STAT functionality.
Original languageAmerican English
Pages (from-to)95-104
Number of pages10
JournalViral Immunology
DOIs
StatePublished - 1 Mar 2016
Externally publishedYes

Fingerprint

Dive into the research topics of 'Upregulation of the suppressors of cytokine signaling 1 and 3 is associated with arrest of phosphorylated-STAT1 nuclear importation and reduced innate response in denguevirus-infected macrophages'. Together they form a unique fingerprint.

Cite this