Not another COVID-19 Variant?! – How viruses evolve and why it’s so difficult to kill them

covid-19, viruses, Not another Covid-19 variant

By Anna Staddon

A new COVID-19 variant has been identified in the UK, similar to the South African strain that officials have been desperately attempting to suppress. 

The strain B.1.525, recently identified through genome sequencing, is causing concern over a mutation to the spike protein named E484K. According to researchers at the University of Edinburgh the mutation could affect the transmissibility of COVID-19.

Since the beginning of the pandemic, emerging strains of COVID-19 have been a constant threat to public health. The UK now has quarantine hotels requiring residents returning from 33 red list countries to spend £1,750 to quarantine for 10 days. The state has started mass testing in hotspots where new strains are identified, and Boris Johnson has identified new strains as one of the four factors affecting the ‘roadmap’ outlined on the 22nd February to relax restrictions. 

So why have we not been able to kill COVID-19 and stop the emergence of new strains? And how do viruses evolve?

What are viruses?

Viruses are a biological anomaly. They do not fit the definition of a ‘living organism’ but are also clearly more than a bundle of inert DNA. With a basic composition of nucleic acid (DNA or RNA) surrounded by a capsid (protein coat), viruses have no organelles, no cell structure, and therefore no apparatus for the metabolic processes that living organisms carry out like protein production and respiration. Viruses can only survive in a host cell, reproducing using borrowed organelles, which in the case of COVID-19 are lung epithelial cells.

Why are they so difficult to kill?

The unique nature of viruses makes them extremely difficult to target. They are tiny compared to other pathogens and with none of the same recognisable structures, cannot be killed under the same pathways.

Aside from physical and chemical barriers, humans have an ‘adaptive’ immune response to protect against infections. Pathogens have specific antigens on their surface that are recognized as foreign upon entry to the human body, triggering B and T lymphocytes to produce specific antibodies that bind to the antigens and inhibit, neutralise or kill the pathogen. It takes time for the immune system to develop specific antibodies, but memory lymphocytes ensure that once they have been produced, future infections are suppressed much faster. For those without a developed immunity, treatment is often needed to combat infection and compared to other pathogens, viruses are tricky to develop treatment for.

Bacteria are targeted by antibiotics which attach to antigens on the surface of a bacterium and target a property that is different to the host cells. The cell components that antibiotics target are often common across types of bacteria so the same treatment can have a widespread application for different bacterial infections. On the other hand, viruses are more varied in composition and require specificity in their targeting, making them difficult to kill.

Viruses don’t have a metabolism but use host cells to reproduce, so it’s difficult to develop treatments that target the pathogen without attacking the host too. To make matters more complicated, viruses are inert outside of the host, allowing them to largely evade detection and targeting.

What treatment is available?

Antiviral drugs are used to treat viruses. They don’t destroy the pathogen but instead inhibit its development by targeting and disabling a viral protein which has a unique structure, meaning that human proteins will not be targeted. The development of new antiviral drugs to help fight the current pandemic is a huge area of research, but still takes a lot of time so pre-existing treatments for Ebola and Malaria have also been trialled for efficacy against COVID-19. Other treatments for COVID-19 have included dexamethasone, a steroid that reduced inflammation and symptoms following infection.

The only way to really ‘kill’ viruses is to suppress levels in the population to a point where any outbreak peters out. This is done by reducing hosts for the virus through herd immunity or vaccination. Vaccines contain a weakened or inactive dose of the virus that triggers an immune response, producing antibodies that build immunity, protecting against viral infection.

So far, only one disease has ever been officially eradicated from the world: smallpox in 1979. However, the vaccines developed for COVID-19 have been the fastest in history, with the world’s first approved vaccine administered outside of clinical trials on the 8th December 2020 in the form of the Pfizer BioNtech vaccine in the UK.

How do viruses evolve?

Variation always exists in a population in the form of DNA mutations. Mutations can be synonymous meaning they are silent and don’t express a physical trait or non-synonymous, coding for a physical variation. Some physical traits will not affect the organism’s survival, but occasionally a random mutation will code for a variation that is advantageous to survival, making the organism ‘fitter’. Natural selection favours advantageous variations (mutations) as individuals with the associated traits are more likely to survive and reproduce meaning over generations, the entire population develops the trait. When a virus is free to spread through a population, there is no reason to favour a mutation. 

However, if there is a high level of natural immunity or if most people have been vaccinated there is a ‘selection pressure’ on the virus to evolve. Virions with a random mutation that codes for resistance against the vaccine or a higher infection rate etc. will be favoured. With a rapid reproduction rate, natural selection acts quickly on viruses and mutations can accumulate over generations rapidly developing new strains.

We have seen this first-hand in the UK. In September the first cases of a new strain were detected that were 70% more infectious, resulting in stricter tier systems and a short lockdown in November. Five months on and we have identified another new strain identified (B.1.525) with a mutation to the spike protein that could potentially help virus particles penetrate lung epithelial cells making the strain more transmissible. Mutations to the virus’s spike protein could lead to increased viral resistance to already developed vaccines since antibodies neutralise virus’s by targeting their spike protein.

The vaccine rollout has been the saving grace of this pandemic, giving us hope for a world where COVID-19 doesn’t dominate our lives. The overriding fear with coronavirus and how it evolves is if a strain will develop strong resistance to any vaccine available. Experts have pointed out that several current vaccines could be easily updated for emerging strains. However, if we want to stand a chance of having a cold pint with friends this summer, we must avoid mutations, avoid infections and prevent the spread at all costs.

Graphic courtesy of Nahal Sheikh