Antiviral viperin protein impairs Junín virus glycoprotein G1 membrane expression

MORELL ML; PEÑA CÁRCAMO JR; CORDO SM; GARCIA CC

Cordoba

Simposio; 2nd Argentinean Symposium of Glicobiology; 2016

Sociedad Latinoamericana de Glicobiología

Junín virus (JUNV) causes Argentine hemorrhagic fever and belongs to Arenaviridae family. Its genome is composed by two single-stranded ambisense molecules of RNA called L and S which codifies for 4 proteins, including viral glycoprotein (G1). G1 is responsible of interaction with host cell receptors and viral endocytosis. We have observed that G1 expression is restricted by viperin (Vip), a type I interferon stimulated gene. Vip antiviral activity was proved through overexpression in A549 JUNV infected cells: virus yield diminished 93% and it was seen a 90% reduction of G1 expressing cells, respect to viral controls. Likewise, number of cells per viral focus was reduced from 93 to 3 in Vip transfected-JUNV infected cells. At the same time, G1 localization was determined in lipid rafts (LRs) in cell plasmatic membrane using a double staining of G1 and LRs markers, cholera toxin and caveolin. A superficial and ring-like pattern of G1 was observed in JUNV infected cells whether in Vip transfected-JUNV infected cells not only a 70% reduction was noticed but an isolated and punctate pattern of G1 was observed. Additionally, when staining G1 in JUNV infected cells, long virus filament projections were revealed whether in Vip transfected-JUNV infected cells a punctate pattern was observed instead. Altogether these results indicate that Vip is an important restriction factor that impairs JUNV G1 membrane expression.