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Journal of Virology, February 2005, p. 1523-1532, Vol. 79, No. 3
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.3.1523-1532.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Blockade of the Poliovirus-Induced Cytopathic Effect in Neural Cells by Monoclonal Antibody against Poliovirus or the Human Poliovirus Receptor

Akiko Yanagiya,^1, Qingmei Jia,^1, Seii Ohka,¹ Hitoshi Horie,² and Akio Nomoto^1*

Department of Microbiology, Graduate School of Medicine, The University of Tokyo, Hongo, Bunkyo-ku,¹ Japan Poliomyelitis Research Institute, Kumegawa, Higashimurayama, Tokyo, Japan²

Received 20 May 2004/ Accepted 19 September 2004

The poliovirus (PV)-induced cytopathic effect (CPE) was blocked in neural cells but not in HeLa cells by the addition of monoclonal antibody (MAb) against PV or the human PV receptor (CD155) 2 h postinfection (hpi). Since each MAb has the ability to block viral infection, no CPE in PV-infected neural cells appeared to result from the blockade of multiple rounds of viral replication. Pulse-labeling experiments revealed that virus-specific protein synthesis proceeded 5 hpi with or without MAbs. However, in contrast to the results obtained without MAbs, virus-specific protein synthesis with MAbs was not detected 7 hpi. Shutoff of host translation was also not observed in the presence of MAbs. Western blot analysis showed that 2A^pro, the viral protein which mediates the cleavage of eukaryotic translation initiation factor eIF4G, was still present 11 hpi. However, intact eIF4G appeared 11 hpi. An immunocytochemical study indicated that 2A^pro was detected only in the nucleus 11 hpi. These results suggest that neural cells possess protective response mechanisms against PV infection as follows: (i) upon PV infection, neural cells produce a factor(s) to suppress PV internal ribosome entry site activity by 7 hpi, (ii) a factor which supports cap-dependent translation for eIF4G may exist in infected cells when no intact eIF4G is detected, and (iii) the remaining 2A^pro is not effective in cleaving eIF4G because it is imported into the nucleus by 11 hpi.

Present address: Department of Biochemistry, McGill University, McIntyre Medical Sciences Building, Rm. 807, 3655 Drummond St., Montreal, Quebec, Canada H3G 1Y6.

Present address: Department of Molecular and Medical Pharmacology, CHS 23-120, University of California at Los Angeles, Los Angeles, CA 90095.

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