A mutant form of the poliovirus receptor (CD155) selected during persistent infection reduces virus-induced apoptosis compared to the wild-type receptor.
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Mutant CD155 attenuates poliovirus-induced apoptosis in vitro; leaves open its contribution to viral persistence in vivo.
Poliovirus (PV) can establish persistent infections in human neuroblastoma IMR-32 cells. We previously showed that during persistent infection, specific mutations were selected in the first extracellular domain of the PV receptor (CD155) of these cells (N. Pavio, T. Couderc, S. Girard, J. Y. Sgro, B. Blondel, and F. Colbère-Garapin, Virology 274:331-342, 2000). These mutations included the Ala 67 --> Thr substitution, corresponding to a previously described allelic form of the PV receptor. The mutated CD155(Thr67) and the nonmutated IMR-32 CD155 (CD155(IMR)) were expressed independently in murine LM cells lacking the CD155 gene. Following infection of the cells with PV, we analyzed the death of cells expressing these two forms of CD155. Levels of DNA fragmentation, caspase activity, and cytochrome c release were lower in LM-CD155(Thr67) cells than in LM-CD155(IMR) cells. Thus, the level of apoptosis was lower in cells expressing mutated CD155 selected during persistent PV infection in IMR-32 than in cells expressing the wild-type receptor.
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Gosselin‐Grenet et al. (2002) studied this question.
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