As viruses are exposed to environmental selection pressures, they mutate and evolve, generating variants which will possess enhanced virulence.
The mutation rate of ssRNA viruses is observed to be much on top of organisms that possess ssDNA, and lots of times over those with dsDNA. Not all mutations necessarily increase virulence, and within the majority of cases may after all be deleterious or inconsequential.
Therefore, organisms must find an equilibrium between a high mutation rate that enables them to adapt to changing environmental conditions, and an occasional one that lessens the incidence of catastrophic mutations. Small DNA viruses may encode their own DNA repair, and a few RNA viruses also share the power to test for and repair replication errors.
However, while DNA viruses generally depend upon the transcription machinery of the host cell, RNA viruses encode for his or her own transcription machinery, meaning that their replication and mutation rate is more directly associated with their own genome and is subject to the identical evolutionary pressures.
Vignuzzi & Andino (2012) note that the offspring of RNA viruses, with genomes commonly falling into the dimensions range of 7-12 kb long, tend in-tuned one or two distinct mutations per nucleotide site. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genome is believed to be around 27-31 kb long, increasing the number of mutations acquired, without necessarily increasing the incidence rate.
The ability to rapidly acquire new genetic characteristics allows viruses to emerge in novel hosts, avoid vaccine-induced immunity, and become more virulent, but may also be a double-edged sword in terms of improving overall genome fitness.
What variants of concern are found?
One new strain with a very sizable amount of mutations was first noted within the UK in September 2020, termed VOC 202012/01 (a variant of concern – December 2020), and also called 20B/501Y.V1by the CDC. This strain is of B.1.1.7 lineage.
Since its identification in Britain, the B.1.1.7 strain has been found in over 90 different countries round the world. what’s concerning about it’s that it’s thought to be 30-50% more infectious than original strains, and will be more deadly. However current vaccines still work on the strain.
The B.1.1.7 strain has the subsequent key mutations:
H69-V70 and Y144/145 deletions
SARS-CoV-2 interacts with ACE2 receptors within the body using its spike protein. This consists of two subunits, the primary of which contains the receptor-binding domain. The B.1.1.7 lineage encompasses a mutation on the receptor-binding domain, specifically with an asparagine organic compound being replaced with tyrosine at position 501, thus the mutation is termed N501Y.
Additionally, the strain often shows a deletion of amino acids 69 and 70, also seen to arise spontaneously in other strains, causing a conformational change of the spike protein.
At position 681, a mutation from a proline organic compound to histidine has also been found to arise spontaneously in several strains and is prominent in B.1.1.7, as could be a mutation to open reading frame 8, the function of which isn’t yet fully understood.
Evidence suggests that this strain is more transmissible, though it doesn’t appear to reduce vaccine efficacy. Recent studies suggest this strain is more deadly, linked to the next chance of hospitalization.
Another strain, B.1.351 (also called 20C/501Y.V2), also shares the N501Y mutation. This variant was first detected in African nation, October 2020, and has been found in additional than 48 other countries since then.
The strain isn’t thought to be more deadly but is more transmissible than the first strain of SARS-CoV-2. Whilst more research is required on the effect of various vaccines on B.1.351, evidence is suggesting a number of this vaccines may have reduced efficacy against this variant.