Key result
Transgenic expression of CD46 in rats allowed measles virus uptake but did not overcome the intracellular block of viral replication, resulting in no measles-like disease.
Transgenic rats expressing CD46 are not a viable small animal model for measles pathogenesis because they exhibit an intracellular block to viral replication despite successful viral entry.
CD46-transgenic rats unsuitable as measles models; leaves open need for better small-animal systems to study pathogenesis.
The study of measles pathogenesis and the testing of improved vaccine candidates is hampered by the lack of a small animal model which is susceptible to infection by the intranasal route. With the identification of CD46 as a measles virus (MV) receptor, it was feasible to generate transgenic rats to overcome this problem. Although there was widespread expression of CD46 in the transgenic Sprague-Dawley rats, no measles-like disease could be induced after various routes of infection. The expressed transgenic protein was functionally intact since it mediated MV fusion and was downregulated by contact with MV hemagglutinin. In vitro studies revealed that CD46-expressing rat fibroblasts take up MV but do not allow viral replication, which explains the nonpermissiveness of the transgenic rats for in vivo infection.
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Niewiesk et al. (1997) studied Measles virus infection. CD46 expression was evaluated on Measles-like disease induction and viral replication. Transgenic expression of CD46 in rats allowed measles virus uptake but did not overcome the intracellular block of viral replication, resulting in no measles-like disease.
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