DELAY OF VACCINIA VIRUS-INDUCED APOPTOSIS IN NONPERMISSIVE CHINESE-HAMSTER OVARY CELLS BY THE COWPOX VIRUS CHOHR AND ADENOVIRUS E1B 19K GENES

The infection of vaccinia virus in Chinese hamster ovary (CHO) cells p roduces a rapid shutdown in protein synthesis, and the infection is ab ortive (R. R. Drillien, D. Spehner, and A. Kirn, Virology 111:488-399, 1978; D. E. Hruby, D. L. Lynn, R. Condit, and J. R. Iiates, J. Gen. V irol, 47:385-488, 1980). Cowpox virus, which canproductively infect CH O cells, had previously been shown to contain a host range gene, CHOhr , which confers on vaccinia virus the ability to replicate in CHO cell s (D. Spehner, S. Gillard, R. Drillien, and A. Kirn, J. Virol, 62:1297 -1303, 1988). We found that CHO cells underwent apoptosis when infecte d with vaccinia virus. The expression of the CHOhr gene in vaccinia vi rus allowed for the expression of late virus genes, CHOhr also delayed or prevented vaccinia virus-induced apoptosis in CHO cells such that there was sufficient time for replication of the virus before the cell died. The E1B 19K gene from adenovirus also delayed vacinia virus-ind uced apoptosis; however, there was no detectable expression of late vi rus genes. Furthermore, E1B 19K also delayed cell death in CHO cells w hich had been productively infected with vaccinia virus. This study id entifies a new antiapoptotic gene from covrpox virus, CHOhr, for which the protein contains an ankyrin-like repeat and shows no significant homology to other proteins. This work also indicates that an antiapopt otic gene from one virus family can delay cell death in an infection o f a virus from a different family.