Key result
Reverse genetics system reveals measles virus protein roles in viral tropism, spread, and pathogenesis.
Why the study?
Pathogenic wild-type measles virus strains differ from laboratory-adapted attenuated strains, and molecular mechanisms underlying MV pathogenicity and adaptation were not fully understood.
The establishment of a highly efficient reverse genetics system for the measles virus enables detailed molecular analysis of viral replication, tropism, and pathogenesis.
Answers are grounded in this paper and cite their sources.
Advances measles reverse genetics tools in animal models; leaves open human translation pending further validation.
In 1990 Kobune et al. succeeded in isolating pathogenic wild-type strains of measles virus (MV) using a marmoset B-lymphoblastoid cell line B95a. Their data indicated that MV strains that have been used in laboratories are attenuated strains through the adaptation to grow in a variety of cultured cells. We have established a very efficient reverse genetics system that allows us to engineer the genome of a wild-type MV strain at will by site-directed mutagenesis or recombination. Using the system it was shown that (1) the H protein determines tropism of MV, (2) the M protein regulates mode of MV spread, (3) the C protein inhibits host innate immune responses, and (4) the long untranslated regions in the M and F genes function to moderate cytopathogenicity by MV. These data advanced our understanding of molecular bases for MV pathogenicity and mechanisms of MV adaptation to grow in cultured cells.
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Makoto Takeda (2007) conducted a review in Measles virus infection. Reverse genetics system for measles virus was evaluated. A highly efficient reverse genetics system for the measles virus was established, revealing the roles of H, M, and C proteins and untranslated regions in viral tropism, spread, and pathogenesis.
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