You may have read that the COVID-19 virus has mutated and that of Spain is not the same as that of Wuhan. But what is true about this? Those who affirm this are supported by the results of a study from the University of Valencia that has been able to read practically all the genetic information of the virus (SARS-CoV-2) from a Spanish patient. Some articles add that this has been the first time that all the genetic information of the virus has been read, however, it is partially false, because its entire genome has been sequenced for weeks and not once, but hundreds of times worldwide . The real novelty to celebrate is that this has been the first time that it has been done with an isolated virus in Spain. And that is the key, because comparing those RNA sequences with those of other countries it has been revealed that those of Wuhan and that of Spain are not identical. Does this mean that it has mutated?
Yes, without a doubt it has mutated, but not as you think. Popularly “mutating” sounds really bad, but it doesn’t necessarily mean that the virus becomes more aggressive or that its transmission speeds up, simply that its genetic material has changed. In fact, sometimes the opposite can happen and the virus becomes “tame”.
Everything mutates. All living things do it, even you. So, you may be mutating right now. The information that has helped you build yourself the way you are, hidden in your genes, is constantly facing change. But, although it sounds overwhelming, that something mutes only means that there have been changes in the structure of its genetic material, in your case the famous DNA and in the case of the coronavirus, in its RNA.
DNA is a molecule made up of two “strands” each coiled around the other and made up of many smaller molecules lined up, like beads on a necklace. These “beads” are called nucleotides and each of them shows an even smaller molecule that differentiates them from each other, the nitrogenous bases. The latter are those famous “letters” that are often spoken of: adenine (A), cytosine (C), guanine (G) and thymine (T). To simplify things we can imagine each of these strands as a very long chain of letters such that thus … GATTACACCGTACTTA … The key is how two of these strands (technically called “strands”) come together to form a DNA molecule.
We cannot unite them in any way, we have to make the letters of one “hook” to those of the other and the truth is that they are somewhat capricious. They have a norm: an A only joins a T and a C joins a G. So, the complementary strand to the one we have written before would be the following:… CTAATGTGGCAGAAT… This is very useful, because DNA has a kind duplicate copy of your genetic information and if any letter of one strand mutates and disappears you can know which one was looking for your partner in the other strand.
In the case of RNA, it happens exactly the same, except for two differences. The first is that instead of thiamine (T) it has uracil (U). The second is that on many occasions it can be made up of a single strand, and this is crucial to understand the mutability of SARS-CoV-2.
Thousands of mutations
Unfortunately, the information stored in these molecules, so relevant to life, can change. There are many reasons why this occurs, from damage caused by ultraviolet radiation from the Sun to small errors that occur during cell division. Sometimes a letter is erased or one is changed to another. The positive part is that, as we said before, we have mechanisms that help us fix these errors, correcting them by looking at the intact thread, which works like the negative of a photograph. But, this trick is not within the reach of single-stranded RNA, which is so called when it consists of a single strand. This is why RNA viruses, like SARS-CoV-2, mutate much more than DNA viruses, like herpes (Herpesviridae).
So yes, the coronavirus has mutated and has differences in its RNA compared to the one that spread in Wuhan, but it is not the only one that has mutated. In fact, almost all countries show some differences in their versions. These changes are very interesting for scientists, but not because they tell us how aggressive they are, we still don’t know how to deduce from their RNA. What you can do is reconstruct a kind of virus family tree, placing each of its variants in it to know how it has spread throughout the world and if the Spanish variant is a descendant of the Italian and the Italian of the Chinese . It is what is technically called a phylogenetic tree. However, there is one important detail. Changes are minimal. Of the approximately 30,000 letters that make up the SARS-CoV-2 RNA of the Wuhan variants, Spanish only changes between 9 and 2 letters.
To tell the truth, it is a minimal difference, practically tiny. So small that we can not say that viruses are different, as has been claimed. The virus that came out of Wuhan and that of Spain are practically identical. It may seem strange considering how much it is multiplying if we think that every time it does, the virus risks mutating, especially thinking that it is RNA and therefore more prone to change. However, the situation is more complex, the format of the genetic information is not the only thing that affects mutability. In the case of the coronavirus, its has a genome that is really large compared to other RNA viruses, and among its 30,000 letters it can afford to allocate some to become more stable. It is as if he had between the pages of his genetic encyclopedia a small chapter explaining how to repair the book in case some of its letters were deleted.
This is why coronaviruses in general and SARS-CoV-2 in particular mutate less than most RNA viruses. In fact, it mutates less than influenza viruses (Orthomyxoviridae). And that’s why, until now, there hasn’t been much talk in the media about the possibility of it mutating, because it was unlikely and there was apparently more relevant information.
But there is more. Because as we have said, mutating does not mean becoming more aggressive, it is simply changing. Some of the 30,000 letters of the SARS-CoV-2 RNA are not too relevant, they can change without making a dramatic difference to the information. However, most are really relevant and have been fine-tuned for many generations to allow the virus to function properly. If the RNA begins to suffer we change randomly, adding letters, duplicating them, deleting them or reversing their order, most likely it will be unreadable and the virus will lose something key to its survival.
For example, let’s randomly change a letter of the word “scientist.” We may be lucky and the “o” becomes an “a” giving “scientific” or an “s” is added at the end and it is “scientific”. In both cases, although the word has changed it has acquired a new meaning that could have an interesting function. However, the most normal thing is that from randomness aberrations arise as “scientific” or “scientific”. That is why the parts of the genome that are key to the survival of a species tend to mutate much less than the rest of the areas and the reason that viruses do not usually become more aggressive lightly, although they accumulate many mutations. It is something that happens, of course, but much less than you usually think. However, at the beginning of the article we said something much more shocking, and that is that a virus can also mutate for good, becoming less lethal. Could this happen with SARS-CoV-19?
Evolution is not progress
Mutations happen randomly, we have already said that and that is why there are many neutral mutations that do not change much. What makes mutations succeed and spread to descendants of a virus, a cow, or yourself is the environment they face. In nature, evolution is not progression, we are not going to get better, we simply change and sometimes, a mutation turns out to be beneficial for the specific environment in which we live. For example, polar bears (Ursus maritimus) They are adapted to snow and their white color helps them camouflage themselves, but it does not make them better than other bears, only better for those conditions. When the North Pole thaws, its advantage will disappear, and if climate change were less rapid than it is, it may give them time to adapt by developing a tone more like that of their brown relatives (Ursus arctos)
That change in climate is a selective pressure that pushes species to evolve and the same is true of viruses. What advantage does a virus get from becoming more deadly? In general, the virus does not obtain any benefit from the death of its host, the damages it causes in our body are often collateral to its true “interest”: entering our cells and taking advantage of the machinery they use to duplicate their DNA for their own benefit. , making copies of its RNA and therefore of itself. This cell hijacking usually leaves sequels that produce fever, inflammation of the airways that makes breathing difficult, and the rest of the symptoms and signs reported by those infected. What really interests the virus is to spread as fast as it can.
Let’s face it, a pathogen doesn’t seek to do harm, but it doesn’t much matter to it either, so there’s no reason to try to avoid it, at least as long as you always have someone else to infect when you kill the first one. In other words: when there is a large population within the reach of the virus, you only feel the selective pressure to transmit yourself faster than the rest of the viruses to “win the race”, even if it comes at the cost of becoming more aggressive and damaging your cells more. These mutations do not suit us, but let’s think about what would happen when the virus has trouble finding other people to infect.
Mutate for “good”
We are simplifying something that is actually much more complex, but it is a way of transmitting a correct idea about how the microorganisms that take advantage of other beings change, be they viruses, bacteria, fungi, etc. Imagine a small population, perhaps a nomadic community of 20 individuals. A virus too fast will infect in a short time at 20 and will run out of new hosts. Unless, of course, they cross paths with another community. But when can that happen? It may not happen in days or weeks, but in months, and the virus dies because either it has already killed its hosts or they have become immune to it. In these cases, the less aggressive variants of the virus keep their host alive longer and are therefore more likely to find a new one to infect. In fact, it is believed that this is how some very long-developing infections, such as tuberculosis (Mycobacterium tuberculosis)
There are many reasons why we must remain in quarantine. The main one is to protect the population from risk and prevent the virus from spreading rapidly from one person to another. Staying at home reduces the number of daily contacts we have and therefore it is more difficult for the virus to jump to other individuals. This reduces the rate of reproduction of the virus (R0) as well as the number of infected, preventing the health system from becoming saturated and therefore lowering the lethality. We are talking about dynamic parameters of the virus, which change even when its genetics are identical, and explain why the virus behaves differently in different countries. No society is the same, we do not take the same precautionary measures and Europe has a higher proportion of elderly people than China, making it more vulnerable to the virus.
However, there could be another benefit derived from the containment measures and that is that, although we know that they are not perfect and some virus will escape quarantine, it will not be any virus. It will be one that has been able to survive a long period of time in a small population, hardly a family nucleus. It will possibly be a less lethal virus than the SARS-CoV-19 average under the same conditions. We could be talking about a beneficial mutation for us.
Be that as it may, social distancing seems to be the most comprehensive measure to face the pandemic. A pandemic that mutates, yes, but that genetically remains the same that came out of Wuhan and that, if we play cards well, we can press it in our favor.
DON’T NECK IT:
- There are indications that, although the variants of the virus among European countries are not significant, in China there were two different strains of which the most aggressive (the L) is the one that has globalized, although in Wuhan this was the least frequent and it was the S who dominated. This statement is based on A study valid, but with limitations that do not allow to determine if their conclusions are correct or if they have been biased by the lack of subjects or some methodological problem. It is necessary to continue studying it.
- Evolution is not progress and the adaptation that makes an individual fitter depends largely on the context.
- There are neutral mutations and adverse mutations for the organism, such as those that cause genetic diseases in our species. Beneficial mutations are very rare, almost as much as passing a test-type exam by answering all questions randomly.
- In any case, improbable things happen if we wait long enough, so SARS-CoV-2 could mutate for the worse. What this article tries to do is put those odds on the table.
- Sanjuán J, Brines J. Theory of Evolution in Medicine. Madrid: Editorial Panamericana Medical; 2010.
- Tang X, Wu C, Li X et al. On the origin and continuing evolution of SARS-CoV-2. Natl Sci Rev. 2020. doi: 10.1093 / nsr / nwaa036
- SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) Sequences. Ncbi.nlm.nih.gov. https://www.ncbi.nlm.nih.gov/genbank/sars-cov-2-seqs/. Published 2020. Accessed March 18, 2020.
- Cann A. Principles Of Molecular Virology. 6th ed. Academic Press; 2015.
- Stearns S, Hoekstra R. Evolution. Oxford [etc.]: Oxford University Press; 2005.