Viral (coronavirus included) mutations are changes in the genetic code of a virus that naturally occur when an animal or person is infected.
What is also important to remember is that every time a coronavirus (for the purposes of this article, SARS-CoV-2) passes from one person to the other, the likelihood of picking up mutations to its genetic code increases.
While mutations in the genetic code are expected to occur over time, it’s essential to monitor those mutations which occur in important areas of the viral genome as it circulates in the population.
Even though several viral mutations may occur as a result of community spread, it is not all the mutations that affect the virus’s ability to spread or cause disease - because these mutations do not significantly alter the major viral proteins involved in infection.
Eventually, these non-essential (passenger mutations) variants are outcompeted by variants with mutations that are more critical for the virus’s survival and infection.
When coronavirus infectious disease (COVID) spread around the globe in 2019 (COVID-19) and most part of this year, many scientists wondered how the deadly virus behind the pandemic might be changing as it passed from person to person.
Initial insights into how ‘chance mutations’ in HIV helped it to evade the immune system, led to the general belief that the same thing might happen with SARS-CoV-2 (the virus that causes COVID-19).
Even though there is currently an avalanche of genetic sequencing of SARS-CoV-2, scientists still have more questions than answers about these mutations. Whilst the current changes in the viral sequence have not raised alarming public-health concerns, studying the mutations in detail could undoubtedly be important for controlling the pandemic.
It could help to pre-empt those mutations that could assist the virus to evade either the immune systems, vaccines or antibody therapies.
Generally, ribonucleic acid (RNA) viruses, such as influenza, HIV and SARS-CoV-2, tend to pick up mutations quickly as they are copied within their hosts, mainly because the enzymes responsible for copying RNA are inherently prone to making errors.
For instance, after the severe acute respiratory syndrome (SARS) virus began circulating in humans, it developed a ‘deletion’ mutation that was believed to have helped in slowing down the spread of the virus.
But current sequencing data on coronaviruses suggest that they change more slowly than other RNA viruses, probably because of the so-called ‘proofreading’ enzyme that inherently corrects potentially fatal copying errors. Even with this slow mutation, scientists have been able to catalogue more than 12,000 mutations in SARS-CoV-2 genomes.