By Karl Maramorosch
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Extra info for Advances in Virus Research, Volume 71
Roos, R. , and Cashman, N. R. (1995). Antibody titer to the poliovirus in blood and cerebrospinal fluid of patients with the post-polio syndrome. Ann. N. Y. Acad. Sci. 753:201–207. Katz, S. L. (2006). Polio—new challenges in 2006. J. Clin. Virol. 36:163–165. , and Nomoto, A. (1989). Determinants in the 50 noncoding region of poliovirus Sabin 1 RNA that influence the attenuation phenotype. J. Virol. 63:1302–1309. Kew, O. , Freeman, C. , et al. (2002). Outbreak of poliomyelitis in Hispaniola associated with circulating type 1 vaccine-derived poliovirus.
Salient questions include: (1) What cells in the gastrointestinal tract are initially infected and act as the source of excreted virus? (2) What is the receptor used by mouse-adapted strains of poliovirus and how can some polioviruses use both mouse and primate receptors? (3) What determines species differences in susceptibility of the gastrointestinal tract to polioviruses? Why cannot PVR transgenic mice be infected by the natural enteric route? (4) Why are neuroadapted polioviruses unable to infect nonneural cells?
What explains the persistence of wild polioviruses in these two foci? 1% of annual total. Under these circumstances, poliovirus would ‘‘fade out’’ during the winter even in the presence of considerable numbers of unvaccinated susceptible children. By contrast, there is very little seasonality in tropical climates (Nathanson and Martin, 1979). (2) In contrast to injected IPV, OPV must infect a vaccinated person in order to produce an immune response. When a group of seronegative susceptible children are fed OPV, most (but not all) will be Confirmed polio cases 8000 6000 4000 Nigeria stops OPV 1 year 2000 0 1998 2000 2002 Year 2004 2006 FIGURE 9 Global incidence of confirmed cases of paralytic poliomyelitis, 1997–2006, cumulated for Africa, Southeast Asia, and Eastern Mediterranean regions [after WHO (2007), with permission].