An integrated genetic‐epigenetic analysis shed light on the mechanisms linking coronavirus disease 2019 (COVID‐19) and cancer

Despite the links between COVID-19 and cancer, the genetic and epigenetic mechanisms underlying these links remain unclear. [...]far, only genetic and epigenetic variants within three COVID-19 receptors, angiotensin-converting enzyme 2 (ACE2), transmembrane serine protease 2 (TMPRSS2), and cathepsin L (CTSL), have been investigated in cancers [ 4]. There were 265 and 184 COVID-19-SNPs identified from the two GWAS studies, respectively (Figure 1b). Since the two GWAS studies were performed in large sample sizes (both n > 3,000), we merged the two sets of SNPs and ultimately identified 426 COVID-19-SNPs (Supplementary Table S1). Non-significant associations were colored in white. Since different COVID-19-SNPs may associate with the same CpG site, we only showed the best-associated COVID-19-SNP for each CpG. (d) Boxplots summarizing methylation differences of each CpG between tumor and normal tissues. RPLP2 is related to the poor overall survival of LUAD patients [ 9]. [...]RPLP2 encodes a ribosomal protein involved in ribosome biogenesis, which can influence innate immune responses to virus infection and shows a hyperactive state in COVID-19 patients [ 10].