Abstract
Viral infection can dramatically alter a cell's transcriptome. However, these changes have mostly been studied by bulk measurements on many cells. Here we use single-cell mRNA sequencing to examine the transcriptional consequences of influenza virus infection. We find extremely wide cell-to-cell variation in the productivity of viral transcription - viral transcripts comprise less than a percent of total mRNA in many infected cells, but a few cells derive over half their mRNA from virus. Some infected cells fail to express at least one viral gene, but this gene absence only partially explains variation in viral transcriptional load. Despite variation in viral load, the relative abundances of viral mRNAs are fairly consistent across infected cells. Activation of innate immune pathways is rare, but some cellular genes co-vary in abundance with the amount of viral mRNA. Overall, our results highlight the complexity of viral infection at the level of single cells.
Highlights
Viruses can cause massive and rapid changes in a cell’s transcriptome as they churn out viral mRNAs and hijack cellular machinery
We focused on cells that derived >5% of their mRNA from virus, since estimates of relative viral gene expression will be less noisy in cells with more viral mRNAs
While we observe a general increase in the amount of viral mRNA over time as expected from bulk measurements (Hatada et al, 1989; Shapiro et al, 1987), there is wide variation in viral gene expression among individual infected cells
Summary
Viruses can cause massive and rapid changes in a cell’s transcriptome as they churn out viral mRNAs and hijack cellular machinery. Cells infected with influenza virus at high multiplicity of infection (MOI) express an average of 50,000 to 100,000 viral mRNAs per cell, corresponding to 5 to 25% of all cellular mRNA (Hatada et al, 1989). Infection can trigger innate-immune sensors that induce the expression of cellular anti-viral genes (Killip et al, 2015; Iwasaki and Pillai, 2014; Crotta et al, 2013). This anti-viral response is another prominent transcriptional signature of high-MOI influenza virus infection in bulk cells (Geiss et al, 2002). Over 70 years ago, Max Delbruck showed that there was a
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