Background Respiratory syncytial virus (RSV) persistent HEp-2 cells are a heterogeneous mixture of viral antigen-positive and -negative variants, and the mechanism through which viral replication evades the innate immune response and becomes latent remains unclear.
Materials and methods RSV persistently infected HEp-2 cells were isolated and the clones were passaged. By using siRNA silence of RIG-I or TRL3, protein levels of SOCS1, SOCS3 and STAT1/2 in the viral persistent cells were checked by western blot, cytokines concentrations in the supernatant of were determined by ELISA, and antiviral genes expression was detected by RT-PCR.
Results The RSV persistent cells always differentiated into two distinct populations characterised by viral permission or resistance respectively. The viral persistent cells produced a low viral titer, resisted wild-type RSV superinfection, and secreted high levels of IFN-β, Mip-α, IL-8 and Rantes. TLR3, RIG-I and SOCS1 were found to be upregulated. The silence of TLR3 decreased the expression of SOCS1 and the secretion of cytokines.
Conclusion RSV persistent cells are in an inflammatory state that the upregulation of SOCS1 is related to the TLR3 induced signalling pathway, which could be associated with viral persistence.