We also evaluated whether increased cell death might contribute to the larger plaques observed following a MHV68.DHS infection. We first measured necrosis by quantifying levels of lactate dehydrogenase released into the media at 16 hpi, but detected no measurable release following infection with any of the viruses ( Figure  S3A ). We next monitored apoptosis by several assays, including measuring caspase activity, and testing for loss of plasma membrane symmetry and increased membrane permeability. While there was a slight, but statistically significant, increase in caspase 3/7 activity following MHV68.DHS infection relative to MHV68.WT or MHV68.MR infection, in all three cases the level was below that observed in mock infected cells ( Figure S3B ), making it unlikely that this is a primary cause of the increased plaque size. Plasma membrane asymmetry was monitored using PE-conjugated Annexin V, which binds to a component of the plasma membrane normally found on the cytoplasmic surface, and membrane permeability was quantified by the nucleotide binding dye 7-Amino-Actinomycin (7-AAD). By flow cytometry we detected no significant increase in Annexin V binding or 7-AAD staining following infection with either MHV68.DHS or MHV8.MR relative to the uninfected control ( Figure S3C ). Collectively, these findings indicate that although a higher percentage of MHV68.DHS infected cells express viral lytic antigens, this does not appear to cause enhanced cell death, nor does it culminate in higher viral titers.