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Additional resources for Advances in Virus Research, Volume 71
Schild, G. , Cann, A. , Almond, J. , and Maizel, J. , Jr. (1985). Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovaccine genome. Nature 314:548–550. , and Enquist, L. W. (2007). In vitro analysis of transneuronal spread of an alphaherpesvirus infection in peripheral nervous system neurons. J. Virol. 81:6846–6857. Fine, P. E. , and Sutter, R. W. (2004). Polio control after certification: Major issues. Bulletin World Health Org.
26:1449–1469. Eberle, K. , Nguyen, V. , and Freistadt, M. S. (1995). Low levels of poliovirus replication in primary human monocytes: Possible interactions with lymphocytes. Arch. Virol. 140:2135–2150. Engle, M. , and Diamond, M. S. (2003). Antibody prophylaxis and therapy against West Nile virus infection in wild-type and immunodeficient mice. J. Virol. 77:12941–12949. 44 Neal Nathanson Evans, D. M. , Minor, P. , Schild, G. , Cann, A. , Almond, J. , and Maizel, J. , Jr. (1985). Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovaccine genome.
The genomes of VDPV are much closer to Pathogenesis of Poliomyelitis 39 their parental OPV strain than they are to wild poliovirus isolates. Because poliovirus genomes evolve at a fairly constant rate, the number of nucleotide differences between OPV and a VDPV isolate can be used to calculate the length of time that a VDPV isolate has been circulating in the human population. , 2005). Because the poliovirus genome is about 7500 nucleotides, it appears that about 75 mutations are introduced in the course of a year, or one new mutation every 5 days.