Heterogeneous nuclear ribonucleoproteins A and B (hnRNPs A/B), cellular
RNA-binding proteins that participate in splicing, trafficking, translation and turnover of mRNAs, have been implicated in the life cycles of several cytoplasmic RNA viruses. Here, we demonstrate that silencing of hnRNPs A1 and A2 significantly reduces the replication of the arenavirus Junín virus (JUNV), the aetiological agent of Argentine haemorrhagic
fever. While acute JUNV
infection did not modify total levels of expression of hnRNPs A/B in comparison with uninfected cells, non-cytopathic
persistent infection exhibited low levels of these cell
proteins. Furthermore, acutely infected cells showed a cytoplasmic relocalization of overexpressed
hnRNP A1, probably related to the involvement of this
protein in virus replicative cycle. This cytoplasmic accumulation was also observed in cells expressing viral
nucleoprotein (N), and co-immunoprecipitation studies revealed the interaction between
hnRNP A1 and N
protein. By contrast, a predominantly nuclear distribution of overexpressed
hnRNP A1 was found during
persistent infection, even in the presence of endogenous or overexpressed N
protein, indicating a differential modulation of nucleo-cytoplasmic trafficking in acute and persistent JUNV
infections.