IMR Press / FBL / Volume 4 / Issue 4 / DOI: 10.2741/tashiro

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Determinants of organ tropism of sendai virus
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1 Department of Viral Diseases and Vaccine Control, National Institute of Infectious Diseases, Tokyo, 208-0011, Japan
2 Department of Microbiology, California State University, Los Angeles, Los Angeles, California, 90032-8201
Front. Biosci. (Landmark Ed) 1999, 4(4), 642–645;
Published: 1 October 1999

Wild-type Sendai virus is exclusively pneumotropic in mice. Protease activation mutants, ts-f1 and F1-R, were isolated from persistently infected tissue culture cells. Additional mutants were isolated from wild-type Sendai virus with phenotypes similar to the pantropic mutant, F1-R. The genome of the mutants was sequenced and mutations were revealed in several proteins encoded by the genes. Three of the six mutations in the fusion (F) proteins were considered prime candidates for the determinant of pantropism. Characterization of the mutants led to the finding that the exchange (Ser to Pro) residue 115 next to the cleavage site of the F protein was the primary determinant that resulted in the enhanced cleavability of the F protein. Another important finding was bipolar budding of F1-R in polarized epithelial cells and mouse bronchial epithelium. This has been attributed to two mutations in the matrix (M) protein, at residues 128 (Asp to Gly) and 210 (Ile to Thr). Thus the determinants of pantropism of F1-R are protease activation of the F protein and bipolar budding attributed to the mutated M protein and enhanced disruption of microtubules.

Sendai virus
Systemic infection
Proteolytic cleavage
Bipolar budding
Organ tropism
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