ROLE OF NEURAMINIDASE IN THE MORPHOGENESIS OF INFLUENZA-B VIRUS

When ts7, a temperature-sensitive (ts) mutant of influenza B/Kanagawa/ 73 virus, infected MDCK cells at the nonpermissive temperature (37.5 d egrees C), infectious virus was produced at very low levels compared w ith the yield at the permissive temperature (32 degrees C) and hemaggl utinating activity and enzymatic activity of neuraminidase (NA) were n egligible. However, viral protein synthesis and transport of hemadsorp tion-active hemagglutinin to the cell surface were not affected. When the cell lysate was treated with bacterial NA, hemagglutinating activi ty was recovered but infectivity was not, even after further treatment with trypsin. It was found that ts7 was defective in transport of NA to the cell surface and formation of virus particles. Analysis of the genomes of non fs recombinants obtained by crossing ts7 and UV-inactiv ated B/Lee showed that ts7 had the h mutation only in RNA segment 6 co ding for NA and the glycoprotein NB. Nucleotide sequence analysis of t he RNA segment revealed that ts7 had four amino acid changes in the NA molecule but not in NB. We suggest that assembly or budding of influe nza B virus requires the presence of NA at the plasma membrane, unlike influenza A virus.