Functions of the mutated NS1 protein of influenza B virus which has a long caroxyl terminal deletion.

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By hetero typic crosses of influenza A and B viruses, we isolated 3 mutants of influenza virus B/Yamagata, which carried deletion mutations in their NS genes, namely, clone 201, AUB2-253 and AWBY-234. Due to a frame-shift downstream, all of them expressed greatly truncated NS1 protein which lacked more than half of the carboxyl terminal portion of the molecule, leaving NS2 intact. To delineate the functions of the NS gene of influenza virus unequivocally, we first prepared a reassortant virus between clone 201 and wild type B/Lee/40, in which only the mutated NS gene of clone 201 was inserted in place of that of B/Lee. As a control, we also prepared a. control reassortant between wild type, Lee/40 and wild type B/Yamagata, in which only the NS gene was substituted with the wild type NS gene of Yamagata. Comparative studies of the two reassortants revealed the following.(1) A large carboxyl terminal deletion of the NSI protein of influenza virus greatly accelerates cell sestruction.(2) Such a deletion mutation does not affect viral protein synthesis.(3) Carboxyl terminal deletion of the NS1 protein alters the mode of VRNA synthesis.The presence of a large amount of subgenomic RNAs within the virion and the occurrence of multiplicity reactivation suggested that a deletion in NS1 protein inhibited efficient elongation of the nascent viral RNA chains.