Characterization of a tissue culture-adapted strain of murine cytomegalovirus (MCMV), the Vancouver strain, which demonstrated altered tissue tropism in mice was undertaken to help understand the mechanism of pathogenesis of cytomegaloviruses. The Vancouver strain grew to a limited extent in the spleen but failed to grow in the salivary glands of inoculated mice. This mutation probably arose during multiple passaging of the parental Smith strain. The Vancouver strain replicated more quickly and produced a greater yield of virus per cycle than the Smith strain , resulting in a larger plaque size. In addition to these phenotypic differences, the Vancouver strain was found to have a 9.4 kb deletion spanning the I I/L junction of the parental Smith strain (0.960 to 0.995 map units), and a 0.9 kb insertion which mapped to the RI K fragment (0.37 to 0.47 map units). Analysis of virus-induced proteins at various times post-infection identified only one major change in Vancouver strain-infected cells, the absence of a 42K protein found in Smith-infected cells at early and late times.


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