The Sendai virus (SeV) V protein is characterized by the unique cysteine‐rich domain in its carboxy‐terminal half which is fused to the amino‐terminal half of the P protein, but its function has remained enigmatic. The V protein‐directing mRNA is generated by a remarkable process known as mRNA editing involving the pseudotemplated addition of a single G residue at a specific septinucleotide locus in the P gene, whereas the unedited exact copy encodes the P protein. Here, we introduced two nucleotide changes in the septinucleotide motif (UUUUCCC to UUCUUCC) in a full‐length SeV cDNA and were able to recover a virus from the cDNA, which was devoid of mRNA editing and hence unable to synthesize the V protein. Compared with the parental wild‐type virus with regard to gene expression, replication and cytopathogenicity in various cell lines in vitro, the V(−) virus was found to be either potentiated or comparable but never attenuated. The V(−) virus, however, showed markedly attenuated in vivo replication capacity in and pathogenicity for mice. Thus, though categorized as a non‐essential gene product, SeV V protein encodes a luxury function required for in vivo pathogenicity.
- Received September 10, 1996.
- Revision received October 7, 1996.
- Copyright © 1997 European Molecular Biology Organization