Omicron’s intrinsic gene-gene interactions jumped away from earlier SARS-CoV-2 variants and gene homologs between humans and animals

Abstract

Background: Omicron and its subvariants have become the predominant SARS-CoV-2 variants worldwide. The Omicron’s basic reproduction number (R0) has been close to 20 or higher. However, it is not known what caused such an extremely high R0 and whether Omicron’s intrinsic gene-gene interactions are different from earlier variants. Objective: Find Omicron’s intrinsic gene-gene interactions and an explanation for the extremely high R0 Omicron infection. Methods: Max-linear competing logistic regression classifier. Results: We found that Omicron’s intrinsic gene-gene interactions jumped away from earlier SARS-CoV-2 variants which can be fully described by a miniature set of genes reported in our earlier work. We found that the gene PTAFR (Platelet Activating Factor Receptor) is highly correlated with Omicron variants, and so is the gene CCNI (Cyclin I), which is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, and frog. The combination of PTAFR and CCNI can lead to a 100% accuracy of differentiating Omicron COVID-19 infection and COVID-19 negative. Conclusions: We hypothesize that Omicron variants were potentially jumped from COVID-19-infected animals back to humans. In addition, there are also several other two-gene interactions, besides PTAFR and CCNI, that lead to 100% accuracy. Such observations can explain Omicron's fast-spread reproduction capability as either of those two-gene interactions can lead to COVID-19 infection, i.e., multiplication of R0s leads to a much higher R0. At the genomic level, PTAFR, CCNI, and several other genes identified in this work rise to Omicron druggable targets and antiviral drugs besides the existing antiviral drugs.

Keywords

• Homologs
• R0
• Druggable targets
• Platelet
• Diabetes
• Immunodeficiency