By Karl Maramorosch
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Extra resources for Advances in Virus Research: Volume 71
It has been questioned whether this is due to localized expression of the PVR perhaps associated with the promoter used in the PVR mice. Zhang and Racaniello (1997) tested this hypothesis by creating PVR transgenic mice in which the transgene was under the control of an enterocyte-specific promoter. Although there was substantial binding of poliovirus to intestinal tissues, the mice were not rendered permissive for oral infection. Likewise, Crotty et al. (2002) used a b-actin promoter that led to expression of the PVR in intestinal homogenates, but did not render mice susceptible to oral infection.
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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.