By Karl Maramorosch
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753:1–412. De Quadros, C. , Hersch, B. , Olive, J. , Andrus, J. , da Silveira, C. , and Carraasco, P. A. (1997). Eradication of wild poliovirus from the Americas: Acute flaccid paralysis surveillance, 1988–1995. J. Infect. Dis. 175(S1): S37–S42. , and Blondel, B. (1997). Persistent poliovirus infection in mouse motoneurons. Journal of Virology 71:1621–1628. Detjen, B. , and Wimmer, E. (1978). Poliovirus single-stranded RNA and doublestranded RNA: Differential infectivity in enucleate cells. J. Virol.
Grazioso, C. , and Halsey, N. A. (2006). Poliovirus excretion in Guatemalan adults and children with HIV infection and children with cancer. Biologicals 34:109–112. , and Blondel, B. (2007). Poliovirus induces Bax-dependent cell death mediated bhy c-Jun NH2-terminal kinase. J. Virol. 81:7504–7516. , and Mayer, C. (2006). Interrupting poliovirus transmission—new solutions to an old problem. Biologicals 34:133–139. Aylward, R. , Sutter, R. , and Heymann, D. L. (2005). OPV cessation—the final step to a ‘‘polio-free’’ world.
Sequencing shows that reversion is either due to reversal of attenuating mutations or due to new compensating mutations (Agol, 2006). The selection for revertant strains implies that the attenuating mutations in OPV strains make them less fit than wild polioviruses for replication in the gut. Presumably, the revertant mutations also enhance neurovirulence, although selection does not involve passage in the CNS. The frequent and rapid reversion of OPV to viruses of enhanced virulence has raised the possibility that VDPV could spread into the community and cause cases of paralytic poliomyelitis.