Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1

Siying Ye; Chris Cowled; Cheng-Hon Yap; John Stambas

The copyright holder for this preprint (which was not peer-reviewed) is the author/funder. . https://doi.org/10.1101/324723 doi: bioRxiv preprint for promoting anti-viral responses, as STING-knockout THP-1 cells produce less type I IFN following 302 influenza A virus infection (39). Reduction of STING gene expression or other anti-viral factors (e.g. 303 IFNB1, MX1, ISG15; Table S1 ) by apocynin, may in part, explain the slight increase of the 304 transcription levels of all influenza genes (NS gene was significantly upregulated) following apocynin 305 treatment (Fig. 2G) . These results also suggest that apocynin treatment may reduce H5N1-induced 306 inflammation and apoptosis. Indeed, the anti-inflammatory and anti-apoptotic effects of apocynin have 307 been shown previously in a number of disease models, including diabetes mellitus (40) could suggest the possibility that upregulation of CEACAM1 (to inhibit NK activity) may be a novel 324 and uncharacterized immune evasion strategy employed by influenza viruses. Our laboratory is now 325 All rights reserved. No reuse allowed without permission.