SARS-CoV-2 - explaining the UK variant of the virus

                                                                                                                         Shutterstock

The emergence of three new variants of SARS-CoV-2 with what appears to be greater transmission amongst human populations again points to the manner in which viruses evolve and adapt in relatively short timespans. The new variants are from the UK (B.1.1.7), South Africa (B.1.351) and Brazil (P.1).  

The engine of SARS-CoV-2 is its ribonucleic acid (or RNA) that is similar to human DNA but more primitive. SARS-CoV-2 spreads by binding to human cells through the spike proteins on its surface that allow it to penetrate cells and fuse its RNA into the target thus enabling it to replicate itself.

As the virus moves from population to population, this process of replication can and does lead to mutations occuring in the RNA which is then passed on to new hosts.

The UK strain of SARS-CoV-2 contains eight mutations to its spike protein of which three are of concern. These three mutations have been designated as -

• N501Y: which enables increased binding to human and murine ACE2 receptors (or the angiotensin-converting enzyme 2 which is found on the surface of human cells)
• 69-70del: which is traced to evolving from the outbreak in farmed minks
• P681H: which is associated with the furin cleavage site (FCS) in the spike protein and enhances what is known as "fusogenicity' or the ability to bind with other cells. The FCS in SARS-CoV-2 appears unique compared to other coronaviruses and more potent.

The efficacy of vaccines currently being deployed in respect of the new strains remains under investigation. The early data from vaccines produced by Johnson & Johnson, Oxford/AstraZeneca and Novavax is not as promising for the UK variant as the original virus although Pfizer appears to be effective.