African green monkey kidney Vero cells require de novo protein synthesis for efficient herpes simplex virus 1-dependent apoptosis

Department of Microbiology, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
Virology (Impact Factor: 3.32). 07/2005; 336(2):274-90. DOI: 10.1016/j.virol.2005.03.026
Source: PubMed


During HSV-1 infection, IE gene expression triggers apoptosis, but subsequent synthesis of infected cell proteins blocks apoptotic death from ensuing. This "HSV-1-dependent" apoptosis was identified in HEp-2/HeLa cells infected with wild-type HSV-1 in the presence of an inhibitor of protein synthesis or a virus lacking ICP27 {HSV-1(vBSDelta27)}. Unlike HEp-2/HeLa cells, vBSDelta27-infected Vero cells fail to exhibit dramatic apoptotic morphologies at times prior to 24 hpi. Here, we examined the basis of these different apoptotic responses to HSV-1. We found that infected Vero cells take substantially longer than HEp-2/HeLa cells to display membrane blebbing, chromatin condensation, DNA laddering, and PARP cleavage. Vero, but not HEp-2/HeLa, cells required de novo protein synthesis to exhibit efficient HSV-1-dependent apoptosis, which included changes in mitochondrial membrane potential, and these factors were produced prior to 3 hpi. Vero cells infected with recombinant viruses devoid of the ICP27 and ICP4 proteins alone or both the ICP27 and ICP22 proteins were apoptotic. These results indicate a requirement for cellular or other viral protein synthesis in Vero cells and provide insight into cell type differences in HSV-1-dependent apoptosis.


Available from: John A Blaho
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    • "Saos-2 is a non-transformed cell line derived from the primary osteosarcoma of an 11-year-old Caucasian girl [50]. HEp2 cells [51] were derived via HeLa contamination. Vero cell line [51] was derived from kidney of a normal adult African green monkey. "
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    • "Additionally, HSV-1 infection induces autophagy in some cells including fibroblasts and macrophages (English et al., 2009; McFarlane et al., 2011). As identifying the HSV-1-induced cell death mechanisms appears to be dependent on differences in cell type (Aubert & Blaho, 2003; English et al., 2009; Galvan & Roizman, 1998; McFarlane et al., 2011; Nguyen et al., 2005), cellular factors may be important for HSV-1-induced cell death and viral replication. Thus, in this study, the effects of axin expression were investigated in terms of HSV-1 replication and virus-mediated cell death to analyse the influence of host factors during HSV-1 infection. "
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