Ascoviruses (AVs) induce a unique pathology in their insect host cells causing cleavage of the cells into virion-containing vesicles. The mechanism by which AVs induce vesicle formation is poorly understood. It is postulated that the virus initially induces apoptosis leading to cell fragmentation. The apoptotic bodies are however, rescued by the virus to form the vesicles. Here we show that Heliothis virescens AV (HvAV-3e) is able to inhibit chemically induced apoptosis from around 16 h after infection. Analysis of the genome of the virus indicated the presence of a putative inhibitor of apoptosis (orf28) gene that encodes a protein with an imperfect baculovirus inhibitor of apoptosis repeat (BIR) and a RING domain. Transiently expressed orf28 did not inhibit chemically induced apoptosis suggesting that the protein may not serve as an inhibitor of apoptosis. Nevertheless, RNA interference studies revealed that the gene is probably essential for virus pathology and replication.