Furthermore, the average magnitude of CPSF30 ChIP-seq signal at the highest expressed B2 SINE loci during infection (Fig. 4A) was twofold higher than the CPSF30 ChIP-seq signal at Pol II-transcribed loci in mock cells (SI Appendix, Fig. S3A) There was also a strong correlation between Polr3A and CPSF30 ChIP-seq coverage at these loci, suggesting that high Polr3A occupancy may contribute to CPSF30 recruitment (Fig. 4C). Here, POLR3A is linked to infection.