Influenza virus intimately associates with host RNA polymerase II (Pol II) and 
mRNA processing machinery. Here, we use mammalian native elongating transcript 
sequencing (mNET-seq) to examine Pol II behavior during viral infection. We show 
that influenza virus executes a two-pronged attack on host transcription. First, 
viral infection causes decreased Pol II gene occupancy downstream of 
transcription start sites. Second, virus-induced cellular stress leads to a 
catastrophic failure of Pol II termination at poly(A) sites, with transcription 
often continuing for tens of kilobases. Defective Pol II termination occurs 
independently of the ability of the viral NS1 protein to interfere with host 
mRNA processing. Instead, this termination defect is a common effect of diverse 
cellular stresses and underlies the production of previously reported 
downstream-of-gene transcripts (DoGs). Our work has implications for 
understanding not only host-virus interactions but also fundamental aspects of 
mammalian transcription.