M. Tashiro¹ and J.T. Seto²

1 Department of Virology 1, National Institute of Infectious Diseases, Tokyo, Japan, 162 and ² Department of Microbiology, California State University, Los Angeles, Los Angeles, California, 90032-8201

Received 11/10/97 Accepted 11/14/97

4. PERSPECTIVES

The determinants of organ tropism and for pantropism of the protease activation mutant, F1-R, are proteolytic cleavage and bipolar budding, attributed to mutations in the F and M proteins, respectively. Proteolytic cleavage permits the virus to undergo multiple cycles of replication in the lungs, the primary site of infection. Bipolar budding facilitates the systemic spread of the virus via the peripheral blood to distant organs where the virus again undergoes multiple cycles of replication. This results in the systemic infection. Wild-type Sendai virus infection is restricted to the lungs whereas F1-R causes systemic infection. We propose that another determinant may be involved is in the enhanced disruption of the microtubules. Further studies are required to determine the mechanism by which the disruption of the microtubules occurs