FIG. 1.

Wild-type influenza A/WSN/33 virus and recombinant WSN-NS1(1-126) virus. (A) Schematic representation of the NS genes and gene transcripts for wild-type (wt) influenza WSN virus and recombinant WSN-NS1(1-126) virus. Viral NS genes are indicated by light gray boxes, with nucleotide (nt) length indicated in numbers below the gene segments. Stop codons for wild-type NS1 and NS1(1-126) open reading frames are indicated by an asterisk above the viral genes. Viral nuclear export protein (NEP) mRNAs are also shown, with spotted boxes representing the specific open reading frames of the viral NEP mRNA transcripts. (B) Growth curves of WSN-NS1(1-126) and WSN viruses on MDBK cells. Confluent cell monolayers in 35-mm-diameter dishes were infected with wild-type influenza A/WSN/33 virus and with the mutant WSN-NS1(1-126) virus at an MOI of 0.001. At the indicated time points, infectious particles present in the media were titrated by plaque assay in MDBK cells. (C) Pathogenicity of WSN-NS1(1-126) virus in mice. Groups of five mice were infected intranasally with either wild-type WSN virus or WSN-NS1(1-126) virus at a dose of 2 × 10⁴ PFU/mouse. In addition, four mice were infected with 2 × 10⁴ PFU of delNS1 virus/mouse. Animals were weighed dailyfollowing infection. The body weights on each day postinfection are given as the percentage of the original body weight (on day 0). The average body weight percentages of animals per group are represented. aa, amino acid.