Abstract
The COVID-19 classification and evolution through its multiple mutations have increased its transmissibility rate up to 70% or more globally, threatening to undermine the promise of a number of emerging medications and vaccines that primarily focus on the immune detection of the Spike trimer. Mutations have been long considered as random events, or mistakes during the viral RNA replication. Usually, what can go wrong will go wrong; therefore, repeated transformations lead to the extinction of a virus. On the contrary, the aggregate result of over 300,000 COVID-19 variants have expanded its transmissibility and infectiousness. COVID-19 mutations do not degrade the virus; they empower and facilitate its disguise to evade detection. Unlike other coronaviruses, COVID-19 amino acid switches do not reflect the random unfolding of errors that eventually eradicate the disease. COVID-19 appears to use mutations adaptively in the service of its survival and expansion. One of the COVID-19 primary strategies is to inhibit the production of interferon type (INF) that is involved in recognizing the virus. The deleterious consequences of the cytokine storm where the CD8+ killer cells injure the vital organs of the host may well be collateral damage, as the blind immune system struggles to annihilate the unidentified COVID-19. It is probable that evolution has programmed COVID-19 with an adeptness designed to debilitate key systemic defences to secure its subsistence. To date the infectiousness of the COVID-19 pandemic is exponentially increasing, denoting the possibility of an even more dangerously elusive, inconspicuous, and sophisticated version of the disease.
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