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Abstract
Although herpes simplex virus type 1 (HSV-1) does not induce apoptosis in infected HEp-2 cells, in the presence of cycloheximide infection induced apoptosis with characteristic morphological changes as well as endonucleosomal DNA cleavage. The induction of apoptosis without de novo protein synthesis suggests that a structural protein of the HSV-1 virion is responsible for the observed apoptosis.
Apoptosis or programmed cell death (PCD) is a type of animal cell death in which cells die by an active cellular process under the control of a genetically encoded cell suicide programme Apoptosis is characterized morphologically by cell shrinkage, plasma-membrane blebbing, chromatin condensation and nuclear fragmentation and biochemically by degradation of chromosomal DNA into oligonucleosome- sized fragments (Kerr & Harmon, 1991) . Although many animal viruses are known to induce an apoptotic response in infected cells (Clem & Miller, 1994; Shen & Shenk, 1995; White & Gooding, 1994), cells infected with wild-type herpes simplex virus type 1 (HSV-1) do not show apoptotic characteristics . However, based on the finding that mutant virus which lacks the γ34.5 gene induces PCD in infected human cells (Chou & Roizman, 1992; Chou et al. , 1994), the lack of apoptosis in the HSV-1-infected cells has been considered to be an outcome of expression of a viral antiapoptosis gene whose product inhibits one of the steps in the virus-induced signalling leading to PCD . Later, HSV-1 was found to carry, as well as the γ34.5 gene, an antiapoptosis gene which can suppress the cellular apoptotic response induced by hyperthermia (Leopardi & Roizman, 1996) or sorbitol treatment (Koyama & Miwa, 1997) .
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