Human 30kb coronaviruses entered through the ACE-2 receptors causing fibrosis of lungs and claimed six million deaths worldwide. Here, we investigated the mutations, deletions and insertions of the recent JN.1 omicron coronaviruses. The 49nt deletions in the 3’-UTR was found in 4997 JN.1 sequences although 26nt deletion was initiated previously in JN.1 as well as BA.5, BF.7, BQ.1 and XBB.1.5 omicron viruses. The 31S spike deletion was initiated lately apart from 24LPP, 69HV, 145Y, 211N and 483V deletions. The important 17MPLF spike insertion was found although few scientists claimed there was no such insertion. we first to compare 3-D structures of spike proteins with or without 17MPLF four amino acids insertion and nine amino acids deletions using SWISS MODELLING. The JN.1 viruses caused a more stable trimeric spike involving Thr342, Lys436, Lys440, His441, Ser442, Gly443, Tyr445, Lys479, Ser489, Tyr490, Arg493, Pro494, Thr495, and Gln501 amino acids to interact with ACE-2 receptors. The cytokine storm was reduced in patients with increased immune evasion due to L455S, F456L and R346T spike mutations in KP.2 variants. The JN.1 8th codon GGA = TGA termination codon mutation was initiated which was demonstrated previously in XBB.1.5 lineages. We also detected few small deletions in the ORF8 gene near termination codon with the formation of few amino acids extended ORF8 protein. We claimed that pre-death changes were initiated in JN.1 COVID-19 lineages and computer-simulation showed that Howard-spike with 17MPLF spike insertion appeared more stable than Oppentron-spike without 17MPLF insertion.