The long term goals are to relate structure-function of influenza and paramyxoviruses, particularly the molecular biology of the pathogenesis of influenza and paramyxovirus infections.
The specific aim i s to establish the molecular basis of infectivity of these viruses. A host range mutant of Sendai virus has been isolated from a persistent infection of tissue cultures. The mutant will productively infect MDBK and MDCK cells whereas wild type Sendai virus will not. Since proteolytic cleavage of the fusion (F) protein is necessary for activating the infectivity, the F gene of wild type, host range mutant, and revertants shall be sequenced. This will entail cloning of the cDNA of the gene into pBR322, subcloned in phage M13, and DNA sequencing carried out by the dideoxy method. By identifying th enucleotide sequences that may be responsible for infectivity, and from the predicted amino acid sequence at the cleavage/activation site, this may provide a means for synthesizing polypeptides for the treatment of paramyxovirus infections.
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| Tashiro, M; Yamakawa, M; Tobita, K et al. (1990) Organ tropism of Sendai virus in mice: proteolytic activation of the fusion glycoprotein in mouse organs and budding site at the bronchial epithelium. J Virol 64:3627-34 |
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| Tashiro, M; Pritzer, E; Khoshnan, M A et al. (1988) Characterization of a pantropic variant of Sendai virus derived from a host range mutant. Virology 165:577-83 |
