Canadian Forest Service Publications
Induction of apoptosis by the Amsacta moorei entomopoxvirus. 2013. Perera, S.; Krell, P.J.; Demirbag, Z.; Nalcaciolglu, R.; Arif, B. Journal of General Virology 94:1876-1887.
Issued by: Great Lakes Forestry Centre
Catalog ID: 34753
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The CF-70-B2 cells derived from the spruce budworm (Choristoneura fumiferana) undergo apoptosis when infected with Amsacta moorei entomopoxvirus (AMEV); as characterized by membrane blebbing, formation of apoptotic bodies, TUNEL (TdT-mediated dUTP Nick-End Labeling) staining, condensed chromatin and induction of caspase 3/7 activity. The apoptotic response was reduced when infected with UV-inactivated AMEV, but not when infected in the presence of the DNA synthesis inhibitor, cytosine β-D-arabinofuranoside. Hence, only pre-DNA replication events were involved in inducing the antiviral response in CF-70-B2 cells. The virus eventually overcomes the host's antiviral response and replicates to high progeny virus titres accompanied by high levels of caspase 3/7 activity. The CF-70-B2 cells were less productive of progeny virus in comparison to LD-652, a Lymantria dispar cell line routinely used for propagation of AMEV. At late stages of infection, LD-652 cells also showed characteristics of apoptosis such as oligosomal DNA fragmentation, TUNEL staining, condensed chromatin and increased caspase-3/7 activity. Induction of apoptosis in LD-652 cells was dependent on viral DNA replication and/or late gene expression. A significantly reduced rate of infection was observed in the presence of general caspase inhibitors Q-VD-OPH and Z-VAD-FMK, indicating caspases may be involved in productive virus infection
Plain Language Summary
We studied the behaviour and growth of an insect virus (Amsacta moorei entomopoxvirus ) that has been isolated from the lepidopteran red hairy caterpillar. The genome of this virus has been completely sequenced. We tested the possibility of culturing it in cell lines present at the Great Lakes Forestry Centre. The cell line CF-70-B2, derived from the spruce budworm, was able to support replication of this virus and we compared it to the more commonly used LD-652 cell line. The virus triggered an infection response and was able to replicate in both cell lines. We also studied the mechanism of cell death by entomopoxvirus infection. Often when cells are infected by a virus, the organism sheds the infected cells to limit the spread of infection (apoptosis). Some viruses are able to counter this reaction and overcome the host’s antiviral response.