Although the replication cycle of parainfluenza virus type 5 (PIV5) is initially severely impaired in cells in an interferon (IFN)-induced antiviral state, the virus still targets STAT1 for degradation. As a consequence, the cells can no longer respond to IFN and after 24−48 h, they go out of the antiviral state and normal virus replication is established. Following infection of cells in an IFN-induced antiviral state, viral nucleocapsid proteins are initially localized within small cytoplasmic bodies, and appearance of these cytoplasmic bodies correlates with the loss of STAT1 from infected cells. hybridization, using probes specific for the NP and L genes, demonstrated the presence of virus genomes within these cytoplasmic bodies. These viral cytoplasmic bodies do not co-localize with cellular markers for stress granules, cytoplasmic P-bodies or autophagosomes. Furthermore, they are not large insoluble aggregates of viral proteins and/or nucleocapsids, as they can simply and easily be dispersed by ‘cold-shocking’ live cells, a process that disrupts the cytoskeleton. Given that during infections, PIV5 will inevitably infect cells in an IFN-induced antiviral state, we suggest that these cytoplasmic bodies are areas in which PIV5 genomes reside whilst the virus dismantles the antiviral state of the cells. Consequently, viral cytoplasmic bodies may play an important part in the strategy that PIV5 uses to circumvent the IFN system.


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vol. , part 9, pp. 2147 - 2156

PIV5 cytoplasmic bodies do not bind RNA probes non-specifically.

When counter-immunostaining cells which had been subjected to hybridization, the diffuse pattern of cytoplasmic staining with anti-NP antibodies was less intense and the PIV5 cytoplasmic bodies were more evident than we had previously observed.

IFN-induced translocation of STAT1 to the nucleus is transient.

Vero cells were infected with PIV5 (W3A), with or without IFN added, which highlighted a cell at the edge of a plaque in which small viral cytoplasmic bodies were detected and in which STAT1 was degraded.

[Single PDF of Figures](258 KB)

A549 and A549/BVDV–Npro cells were or were not pretreated with IFN for 18 h prior to infection with W3A. A high-resolution version of this figure is available here(4 MB).


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