SARS-CoV-2, like other viruses, evolves, meaning that its genetic material changes over time. We already know that viral variants are the usual way of things, because we get flu shots each year to cover new viral strains that arise from mutations.
Typically, viruses change or mutate their genetic code as they replicate, altering their proteins, sometimes to give them an evolutionary advantage. It’s a classic example of survival of the fittest. of Certain mutations improve a virus’s chances for survival by making it more contagious or enabling it to evade the immune system. However, some changes can also make them deadlier.
But because the virus survives by living in one host before jumping to the next, it’s actually better for the virus to keep the hosts alive. A deadly virus won’t last long if there are no hosts to infect.
Mutation and the Spike Protein
Viruses generally mutate slowly, but the speed depends on the numbers of hosts infected. The more people infected, the higher the chance that the virus will change. There are already thousands of SARS-CoV-2 mutations, which are mainly inconsequential. But others have changed the virus’s behavior, and those are the ones that concern us.
As the pandemic evolved over the last year, we’ve learned that the SARS-CoV-2 spike protein was crucial for viral attachment and entry into our cells, and that antibodies directed against the spike protein block the virus entering the body. That’s why all the current vaccines target this protein, and push us to produce anti-spike protein antibodies to protect ourselves from getting sick with COVID-19.
If mutations to the spike protein make it less able to attach and enter our cells, the virus is less contagious. But the opposite could also happen – a mutation could make the protein attach better and make it easier for SARS-CoV-2 to gain entry, which could cause a more contagious and potentially deadlier variant. Other mutations can increase the number of viruses in the nose; can increase the amount a person sheds, extend the time a person is contagious, or make the virus more stable in the environment, which would increase the spread of COVID-19. The virus can also mutate in a way that changes the spike protein so that it can no longer be detected with PCR tests.
By sequencing the SARS-CoV-2 genetic material, we can follow its evolution and study the mutations to determine transmissibility or resistance to vaccines. There are a handful of mutants that seem to be taking over and all of them affect the spike protein.
The Main Mutant Strains
The UK variant called B.1.1.7 has 17 changes with 8 of them in the spike protein. The variant causes over 50% more COVID-19 spread than other strains and increases the severity and mortality of disease. Researchers discovered neutralizing antibodies against the B.1.1.7 – now spread to over 75 countries and present across Austria – in serum from people who had a COVID-19 vaccine, which shows that the vaccine protects against this variant.
The South Africa variant, called B.1.351 shares some similar mutations, which increases its transmission. Now dominant in South Africa, it is currently the cause of COVID-19 in Tyrol. This variant has several mutations in the spike protein, improving its binding to our cells and making it 50% more infectious. The main concern is that it reduces antibody binding to the spike protein, so that the current vaccines may not be fully protective.
The Brazilian variant or the P.1 lineage, also known as 20J/501Y.V3 accounts for a large percentage of cases in the Amazon and has spread to other countries, though not yet to Austria. This variant also has mutations in the spike protein, raising concerns about transmission, its ability to escape neutralizing antibodies, and vaccine efficacy.
In the USA, researchers are also following variants, and with their high numbers of infections, it’s likely that the numbers of mutants will increase.
Origin of the Mutants
It’s hard to figure out where and how the mutants originate, especially with the UK variant, which has 17 significant mutations. Typically, coronaviruses evolve slowly by incorporating small genetic errors when they replicate. SARS-CoV-2 has a protection mechanism that allows them to reduce these mistakes by producing special proteins that detect and correct genetic errors. This makes SARS-CoV-2 slower to mutate than the flu, and its adaptations tougher to understand.
One theory is that variants originate from a single person. Most people have COVID-19 for about 14 days, though some people may be contagious for up to 20 days. The usual cycle starts with the SARS-CoV-2 virus quickly infecting our cells, entering our body, making us sick as it replicates. Then the virus moves to the next persons and starts the next cycle. However, there are rare patients with chronic COVID-19 infections, lasting for months. The long period of infection provides the virus with enough time to acquire genetic changes. SARS-CoV-2, like other viruses including Ebola and poliovirus can hang around for a long time within people, who might continuously shed the virus. The patients at risk of chronic infections are immunocompromised, and that makes getting rid of the infection difficult. They can only partially eliminate the virus, which provides evolutionary pressure for the virus to mutate to make it stronger – like having more time to figure out how to resist the immune system and become more contagious.
Vaccines and Variants: What This All Means
Chronic infection may explain the origins of new mutants. Still, the main problem is an ‘out of control’ pandemic with billions of infected people, and thus billions of replicating viruses. The numbers of new variants will increase as the pandemic continues. It’s critical to quickly identify new mutants by extensive genomic surveillance combined with epidemiology – i.e. by contact tracing.
The only way to control the virus and reduce new mutants is to maintain current restrictions. Even though vaccines will help reduce infections and hospitalizations, they will not defend us against the emergence of new variants. Indeed, widespread transmission in a partially-vaccinated population might even generate more mutants able to evade vaccine protection.