Superinfection exclusion is absent during acute Junin virus infection of Vero and A549 cells.

Raphaël Gaudin,Tomas Kirchhausen

doi:10.1038/srep15990

Abstract

Many viruses have evolved strategies of so-called “superinfection exclusion” to prevent re-infection of a cell that the same virus has already infected. Although Old World arenavirus infection results in down-regulation of its viral receptor and thus superinfection exclusion, whether New World arenaviruses have evolved such a mechanism remains unclear. Here we show that acute infection by the New World Junin virus (JUNV) failed to down-regulate the transferrin receptor and did not induce superinfection exclusion. We observed that Vero cells infected by a first round of JUNV (Candid1 strain) preserve an ability to internalize new incoming JUNV particles that is comparable to that of non-infected cells. Moreover, we developed a dual infection assay with the wild-type Candid1 JUNV and a recombinant JUNV-GFP virus to discriminate between first and second infections at the transcriptional and translational levels. We found that Vero and A549 cells already infected by JUNV were fully competent to transcribe viral RNA from a second round of infection. Furthermore, flow cytometry analysis of viral protein expression indicated that viral translation was normal, regardless of whether cells were previously infected or not. We conclude that in acutely infected cells, Junin virus lacks a superinfection exclusion mechanism.

Highlights

Characterized in a model of chronic infection, but whether it occurs during the acute phase of Junin virus (JUNV) infection remains to be determined
Cells acutely infected by a first round of JUNV infection are still fully permissive for virus internalization, viral RNA synthesis, and translation of viral proteins associated with a second round of JUNV infection harbouring the same Candid[1] surface glycoprotein complex (GPC)
Vero cells were infected at a multiplicity of infection (MOI) of 0.1 and superinfected 16 h later with JUNV particles complexed to an Alexa Fluor 647–labelled non-neutralizing antibody[14,15] to allow visualization of the cell-associated virus particles related to the second round of infection

Summary

Introduction

Characterized in a model of chronic infection, but whether it occurs during the acute phase of JUNV infection remains to be determined. Cells acutely infected by a first round of JUNV infection are still fully permissive for virus internalization, viral RNA synthesis, and translation of viral proteins associated with a second round of JUNV infection harbouring the same Candid[1] surface glycoprotein complex (GPC).

Results

Conclusion