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Why the Mutation That Made SARS-CoV-2 More Infective Isn’t That Big a Deal

Why the Mutation That Made SARS-CoV-2 More Infective Isn’t That Big a Deal

Image: qimono/pixabay.

What is a virus? Ask any virologist, and she will likely say something like the following: A virus is an obligate parasite that possesses its own genetic material, but is incapable of independent transcription and translation. That is, a virus is a life-form that relies on its host’s cells to make more copies of itself. Outside the host, it does nothing – rather, it can’t do anything. It is inert. One could even say it is dead, and until it manages to infect a new host, it remains dead. This process forms the core of what viruses are.

When Martinus Beijerinck realised in the late 1800s that there are life-forms smaller than bacteria that can cause infection, the scientific world realised it had an entirely new world to explore. At the centre of this world is the fact that these life-forms are not always alive.

When a virus infects its host cell, it hijacks a part of the cell’s internal machinery to serve its own needs. The cell now has to perform its own functions as well as those of the virus. The virus carries a set of instructions – through its genetic material, DNA or RNA – on how to make more copies of itself, a process that scientists call replication. This is mostly what a virus wants from its host: a place to replicate until it can transmit.

The transmission is necessary because of two reasons. First, the process of replication takes a toll on the host. When that toll is high enough, the virus ends up killing the infected individual. The death of the host is an unfortunate consequence of the viral infection, and it is detrimental to both the host and the virus itself. So the virus must establish a new infection before it destroys its present host. This is hardwired in the virus’s DNA (or RNA).

A virus that can’t transmit before it kills can’t continue to exist forever. Proof of this statement lies in the fact that viruses that can kill quickly, in a matter of weeks – such as Ebola and influenza – are all transmitted very quickly. They have to in order to avoid extinction. The converse is also true: HIV takes years to kill, and it also has more sophisticated modes of transmission that are unlikely to infect a large number of people in a short span of time.

The second reason that a virus must transmit is that if the virus doesn’t kill the host, it means the human immune system has eliminated the virus before it can be a threat. The immune system has two primary functions: to protect and to remember. Once a virus has invaded a host, the immune system will attempt to take all the necessary steps to hunt that virus down. So in order to survive, the virus must transmit to a new host or find another means to survive.

The process of surviving this ‘hunt’ requires that the virus go incognito – in the sense that it must hide its identity so the immune system can’t identify it.

Also read: The Novel Coronavirus Story so Far, From Virology’s Point of View

The immune system recognises these viruses in a series of steps – recognise, track down and destroy. The ‘recognition’ step occurs through the identification of viral proteins. Once identified, the immune system then produces cells to find the virus. A mutation in the viral DNA or RNA will alter the shape of the protein, such that the immune system’s cells can no longer identify the virus. It must now go one step back and begin the identification again.

So in the process of making copies of itself, the virus has evolved to make errors. In technical parlance, it must mutate. A mutation is a change in the DNA (or RNA) of the virus – a change in the instructions about how to make a new virus.

The original set of instructions that the virus carries are the result of hundreds of years of optimisation. A change in this set can be good, bad or neutral depending on the circumstances. The good and bad changes are almost always associated with a cost. For example, the price for escaping the immune system could be a loss or a defect in one of the virus’s other functions. Alternatively, the cost of increasing the ability to infect target cells could be that the virus becomes more easily found by the immune system. All viruses accumulate some mutation or other when they infect a host. It is only natural.

A recent flurry of reports on mutations of the SARS-CoV2 coronavirus – particularly the D614G mutation – have sounded as if the new mutation is straight out of a sci-fi thriller (you can find one example on the website These reports are disturbing because they add to the already alarming levels of panic among people. The D614G mutation has been described mostly in the superlative, with some reports going so far as to reconsider the efficacy of upcoming vaccines.

First off, the chances that a vaccine will not work due to a single amino acid (building blocks of protein) changing is very, very, very low. (In the case of D614G, aspartic acid, code ‘D’, changes to glycine, code ‘G’, at the 614th position – thus ‘D614G’.) This is because vaccines are never designed to target only one small region of the virus. They always use multiple targets to elicit an immune response.

Second, and more importantly, a SARS-CoV-2 virus with the D614G mutation is more infective in laboratory tests. But this does not mean it will spread at the same rate in the population. The results of tests conducted in the laboratory in a cell culture model can’t be directly extrapolated to the real-world. This is because a lot of additional factors are involved in human transmission, including – but not limited to – host-pathogen interactions, host genetics and other epidemiological considerations that don’t exist in the cell-culture model.

Besides, this mutation does not seem to affect the virus’s virulence – i.e. that it may be able to spread a little more effectively but the severity of the disease, COVID-19, won’t change. In essence, it makes no difference to the common person if the virus infecting them contains the D614G mutation or not.

The word ‘mutation’ has always carried a negative vibe. This may be due to a combination of their portrayal in films plus their role in a number of diseases. Many journalists have often sensationalised their occurrence.

Also read: What Stories Do the Symbols of the New Coronavirus Tell Us?

However, for a virologist, news of a mutation in an RNA virus – like the SARS-CoV-2 virus – is as surprising as news of rain in Meghalaya. They are so commonplace, and are many times associated with an infinite beauty. Everyone can behold that beauty when we realise that mutations are indispensable to life, and their occurrence is a reminder of the very essence of evolution. They are also the primary reason that something like viruses exist and live the way they do – through an incessant dance across life and death.

Arun Panchapakesan is a molecular biologist working in the HIV-AIDS laboratory at the Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru.

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