Mammalian orthoreovirus infection is enhanced in cells pre-treated with sodium arsenite

Michael M. Lutz; Megan P. Worth; Meleana M. Hinchman; John S. L. Parker; Emily D. Ledgerwood

to the enhanced viral replication we saw following pre-treatment with SA, heat shock 402 (HS) pre-treatment did not enhance viral replication. Heat shock also activates HRI, but 403 to a qualitatively lower level than SA and with a different pattern of autophosphorylation 404 of HRI [7] . Why pre-stressing cells with SA, but not with heat shock, benefited viral 405 replication is unclear. It is possible that the kinetics, magnitude and timing of eIF2α 406 phosphorylation following these different stressors varied leading to the different 407 outcomes we saw. Alternatively, we cannot rule out the possibility that SA treatment 408 activates responses not mediated by HRI that benefit viral replication. The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/555367 doi: bioRxiv preprint is likely that different strains of reovirus induce SG to varying extents, and that this is 415 influenced by cell type and MOI, our data using the type 3 Dearing strain suggests that 416 infection with this strain of reovirus results in a low level of SG induction that is absent at 417 late times post infection. The timing of SG appearance (peak at 6 h) and dissolution 418 may in fact have been viral factories that were co-staining for the presence of TIAR [15] . 426