Stepping into the 3rd year of COVID-19 pandemic, most of us are expecting what the next new SARS-CoV-2 variant will be. We are told that the more mutations occurring in a variant, the more severe the disease will be, and also the death. Though it seems to be reasonable, the SARS-CoV-2 omicron seems to overrule the high death numbers. The sudden death rising in India (May-June 2021) is incomparable to early South Africa and UK (November-December 2021) mortality cases. This tendency can not be concluded by vaccination or natural infection statuses. Per end of January 2022, Indonesia Omicron death cases were 5 people, three were unvaccinated and two had been vaccinated (one with booster), all of the deceased patients had comorbidities. High positive cases are far outcompeting the mortality.
Sharing Symptoms
Reading prepandemic literatures about common human coronaviruses, one may conclude that Omicron SARS-CoV-2 shares some similar symptoms with common human coronaviruses. According to McNamara1 et al., Human coronavirus (HCoV) strains 229E and OC43 have been long recognized as the second main cause of the common cold (10–25%). Together with NL63 and HKU1, these viruses are ubiquitous and regularly detected in respiratory specimens of a small proportion (1–10%) of children hospitalized with acute respiratory disease in many parts of the world. Infection with these human coronaviruses may present as an upper respiratory tract infection, asthma exacerbation, acute bronchiolitis, pneumonia, febrile seizures and also as croup (especially NL63). Reinfection is common due to rapidly decreasing antibody levels.
Two interesting things about Omicron pathogenesis are the higher reinfection cases and children admission rates. Looking at a 35 years of Coronaviruses reinfections study2 by measuring antibodies to the carboxyl (C)-terminal region of the nucleocapsid protein (NCt)—an immunodominant region of the structural coronavirus capsid proteins, researchers concluded that reinfections by natural infection occur for all four seasonal coronaviruses (HCoV-NL63, HCoV-229E, HCoV-OC43, and HCoV-HKU1), suggesting that it is a common feature for all human coronaviruses, including SARS-CoV-2. Reinfections occurred most frequently at 12 months after infection, indicating that protective immunity is only short-lived. The team warned, “Caution should be taken when relying on policies that require long-term immunity, such as vaccination or natural infection to reach herd immunity.” This includes SARS-CoV-2.
Children positive and admission cases tendency in Omicron is slightly higher than the previous SARS-CoV-2 variant. This may be due to the interferons (IFNs) response similarly found in hCoV. In previous variants, SARS-CoV-2 was known to suppress the IFNs. Though a preprint suggested that Omicron has gained an elevated capability to suppress IFN-beta induction upon infection and to better withstand the antiviral state imposed by exogenously IFN-alpha, the data were from 24 hours after the infection.
Common Cold HCoV Insertions in Omicron
Another study3 suggested that there is a possibility of co-infection or recombinant between common cold HCoV and SARS-CoV-2 variant before Omicron. The authors considered a variety of host-viral and inter-viral genomic matter exchange scenarios that may have contributed to the adoption of INS214EPE mutation in the precursor variant of Omicron. This insertion has never been found in previous SARS-CoV-2 variant. They BLAST-ed to identify the homologs to nucleotide sequence encoding the particular insertion. They found that two different nucleotide sequence insertions can give rise to the sequencing encoding Omicron’s INS214EPE. The search against human coronaviruses — HCoV-OC43 (taxid:31631), HCoV-229E (taxid:11137), HCoV-NL63 (taxid:277944), HCoV-229E (taxid:11137) — resulted in 709 hits.
Virus-Virus Interaction
Dee4 et al. showed that human rhinovirus (HRV) triggers an interferon response that blocks SARS-CoV-2 (GISAID accession no. EPI_ISL_407073) replication, “Mathematical simulations show that this virus-virus interaction is likely to have a population-wide effect as an increasing prevalence of rhinovirus will reduce the number of new coronavirus disease 2019 cases.” HRV is known to reduce the influenza A virus (IAV) by inducing IFN response. When the two viruses were infected together, HRV titers displayed the same kinetics in single infections and coinfections: they increased rapidly during the first 24 hours, followed by a gradual and sustained decline. HRV hampers SARS-CoV-2 replication, even when the former was inoculated 24 hours after SARS-CoV-2. The researchers demonstrated that viral interference interactions induced by HRV infection can inhibit SARS-CoV-2 replication in the respiratory epithelium.
Conclusion
In May the SARS-COV2 OMICRON Variant Signal the End of the Pandemic – A Fibonacci Fractal analysis5, we propose that the Omicron 21K sub-clade, its long-range metastructures of 1797 and 2584 UA/CG lengths tend to disappear marking the disruption of the virus genome fractal cohesion, in relation with a loss of RNA secondary structure conformation (hairpin loops) in this particular gene. This may be the signal to end this COVID-19 pandemic. Our another analysis stated that vaccines may have challenged Omicron by comparing countries with vaccine percentage and case numbers. High vaccine percentage countries tend to have higher Omicron cases. Omicron relations with common cold HCoV and Rhinovirus may relate with the low death numbers and higher children positive cases. These facts lead author to see that Omicron was intentionally created. The purposes may either to end this pandemic, to lower the SARS-CoV-2 pathogenesis, to change SARS-CoV-2 into seasonal common cold (higher reinfections) in order to sustain the selling of the vaccines as almost every country promotes its mandatory.
https://www.sciencedirect.com/book/9780323401814/principles-and-practice-of-pediatric-infectious-diseases?via=ihub=#book-description
https://www.nature.com/articles/s41591-020-1083-1.pdf
https://osf.io/f7txy/
https://pubmed.ncbi.nlm.nih.gov/33754149/
https://www.researchgate.net/publication/357675543_May_the_SARS-COV2_OMICRON_Variant_Signal_the_End_of_the_Pandemic_-_A_Fibonacci_Fractal_analysis
Omicron: Common Cold or COVID-19?
I can't find it anywhere, if Omicron elicits a higher level of Interleukin 35 expression, yes, it was created to literally out compete and end the pandemic for whatever trade off that will entail to our future.