We’re faced with another set of new words: mutation, variant and strain.

So, what do they mean?

The genetic material of SARS-CoV-2, the coronavirus that causes COVID-19, is called ribonucleic acid (RNA). To replicate, and therefore establish infection, SARS-CoV-2 RNA must hijack a host cell and use the cell’s machinery to duplicate itself.

Errors often occur during the process of duplicating the viral RNA. This results in viruses that are similar but not exact copies of the original virus. These errors in the viral RNA are called mutations, and viruses with these mutations are called variants. Variants could differ by a single or many mutations.

Not all mutations have the same effect. To understand this better, we need to understand the basics of our genetic code (DNA for humans; RNA for SARS-CoV-2). This code is like a blueprint on which all organisms are built. When a mutation occurs at a single point, it won’t necessarily change any of the building blocks (called amino acids). In this case, it won’t change how the organism (human or virus) is built.

On occasion though, these single mutations occur in a part of the virus RNA that causes a change in a particular building block. In some cases, there could be many mutations that together alter the building block.

A variant is a referred to as a strain when it shows distinct physical properties. Put simply, a strain is a variant that is built differently, and so behaves differently, to its parent virus. These behavioural differences can be subtle or obvious.

For example, these differences could involve a variant binding to a different cell receptor, or binding more strongly to a receptor, or replicating more quickly, or transmitting more efficiently, and so on.

Essentially, all strains are variants, but not all variants are strains.

Let’s look at the UK variant as an example. This variant has a large number of mutations in the spike protein, which aids the virus in its effort to invade human cells.

The increased transmission of the UK variant is believed to be associated with a mutation called N501Y, which allows SARS-CoV-2 to bind more readily to the human receptor ACE2, the entry point for SARS-CoV-2 to a wide range of human cells.

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