Unfortunately, Spain lives a alertness, marked by the arrival and expansion of the new coronavirus. We emphasize that it is important to follow the sanitary norms that are sent to us by the Government, and to have the social responsibility to be able to carry out the quarantine correctly. Not so much for us as individuals, but for the population at risk that can be greatly affected by this new disease.
But no matter how hard we try to stop the epidemic with our actions, we have been working for three months to achieve some treatment or vaccine that can stop the coronavirus. In this article, we discuss the latest developments in this direction. Hopefully this text will expire soon when you find an available treatment.
Know your enemy
The term coronavirus really is not very informative on a scientific level. A coronavirus is a type of virus rather than a virus itself. All coronaviruses receive this name because when viewed under the electron microscope, proteins appear as threads protruding from the virus envelope, imitating a solar corona (and not a royal corona, as is commonly thought).
Before our famous coronavirus, we actually had seven different types of coronaviruses in circulation. Five of them have been known since the 1960s, and they fall into a huge category we call cold viruses. The cold as such does not exist, but is a whole variety of viruses with common symptoms that we all know, capable of infecting us from time to time. These five coronaviruses are capable of causing mild respiratory symptoms such as runny nose and cough; without becoming excessively serious except in patients with a special risk, such as the elderly, patients with respiratory failure or immunosuppressed patients.
But not all coronaviruses are the same. Although we already knew about these five benign types, in the last twenty years new coronaviruses have emerged that are much more aggressive and whose symptoms cannot be considered a cold. Many will remember the SARS epidemic that struck China and part of the world between 2002 and 2003, or the MERS epidemic that erupted in Saudi Arabia in 2012. Both are coronaviruses, much more aggressive mutated versions and more worrying symptom producers, with lethality. of 10% in the case of SARS and a lethality of 35% in the case of MERS, always affecting the population at risk much more than the rest.
Our current coronavirus was baptized by scientists as SARS-CoV-2. Its name indicates the great similarity with the SARS virus, since 82% of its genome is identical. But this similarity is not complete, since SARS treatments do not work in the fight against the coronavirus. The key is in that remaining 18%, and it is precisely there where the possible targets are to create a vaccine or treatment.
The changing virus
Since it was detected in December 2019, one of the researchers’ first goals has been to describe the virus in great detail. This type of virus is made up of two fundamental parts: an outer envelope, and a small sequence of genetic information inside.
The genetic information of our coronavirus is an extremely long chain of RNA, which includes everything the virus needs to invade a cell and create copies of itself. Once this RNA enters our cells, it is capable of tricking it into manufacturing the proteins that make up the virus and generating copies to wear down the cell and invade new cells.
If we know exactly this RNA sequence, we will know what proteins make up the virus and what it needs to invade the cell, so we can create drugs and vaccines dedicated to preventing its operation. In this sense, we should not focus on the entire genome of the virus, but only on that 18% that is different from SARS and that makes it immune to our treatments.
But there is a problem, viruses easily change genetic information. Every time they create copies inside the cells, changes in the RNA accumulate, making the coronavirus from two months ago in China slightly different from the coronavirus that is now in Spain. For this reason, many scientists have contributed their bit by describing the genetic information from their own coronavirus samples and sharing it with other scientists to find the differences.
In this way, we currently know three weaknesses of the virus, essential for the coronavirus to work and that have not changed in any of the viruses that we have investigated, since if they change the virus stops working. If our bodies or a new drug manages to attack one of these targets, we will no longer be affected by the virus.
One of them is an ORF3b protein, which is capable of stopping the production of interferon within our cell. Interferon is a compound that acts as the first viral protection barrier within our cells and prevents a newly arrived virus from reproducing. For this reason, the coronavirus has a kind of “shield” to prevent interferon from forming, but if we manage to knock it down, the virus will be defenseless against our cell.
The second is a region of the viral RNA, called ORF8, which seems essential for the virus to take over our cellular machinery to reproduce. A team of scientists has already proven that if the virus is modified so that it does not have this region, it becomes incapable of infecting other cells, so it is to be expected that it is essential for its operation.
And the last target is a protein from the outer envelope of the virus. This envelope, called a capsid, is made up of different proteins that fulfill the function of tricking our body’s defenses to “disguise” themselves as human cells, and also recognizing other human cells to attack them. One of the proteins that make up the crown has a part called S2, which is common in all the coronaviruses found and is essential for the virus to attack.
With these three targets, the goal now is to create an effective prophylactic or treatment. To obtain it quickly, the best option is to generate a vaccine, and make our body be in charge of attacking that target.
In search of the best vaccine
The vaccines were born from a deceptively simple idea: injecting a weakened version of the pathogen that does not spread too fast and that leaves time for our defenses to create antibodies against the microbes and immunize us. This may work for certain slowly changing pathogens, but some viruses like coronaviruses change too quickly over time, and adapt to defenses. For this reason we find it difficult to find vaccines for some viruses such as ebolavirus, or we end up creating a temporary vaccine that we must update at the same rate as the virus changes, as in the case of seasonal flu.
If we want to create an effective and fast vaccine, we need to make it easy for the body, and make it accurately recognize the targets of the virus that we have detected, since as we have said, they cannot change. In this way, we will make life impossible for the virus, since we force it to have to change something that in principle it cannot change. For this reason, identifying the targets is the first step in creating any treatment, and we have already achieved this.
Normally making a vaccine is a slow scientific procedure, which requires between fifteen and twenty years. It is not as easy or fast as it appears in movies. The reason is that manufacturing requires a whole series of steps and procedures to obtain an effective vaccine without side effects. It must first be tested on infected experimental animals and then passed on to humans, through several highly controlled clinical trials with more and more subjects. If in any of these intermediate steps it is detected that the possible vaccine has any negative side effect or that it does not create immunity against the virus, it is necessary to start the process from scratch. So it takes so long.
In the war against the coronavirus, many research centers began to carry out experiments with animals since February to realize a new obstacle: the experimental mice are not sensitive to the coronavirus, since the virus does not get to invade their cells.
They already had this same problem during the SARS epidemic and the solution was to make transgenic animals that express some human proteins to trick the virus into deciding to infect them. The scientific community has already generated transgenic animals sensitive to coronavirus but it has taken time, because of course, mice must grow and we cannot accelerate this too much. Right now, several universities in China and Australia already have their coronavirus-sensitive litters and are starting to test possible vaccines.
In parallel, several research centers such as the United States Institute of Allergy and Infectious Diseases are testing simple versions of vaccines with the virus’s target proteins that we have described, hoping that they will work well the first time and without side effects. As an exceptional situation and to speed up the process, these trials are already directly in humans, but they are highly controlled and with few subjects, something necessary if we want to ensure the safety of the possible vaccine.
In short, it is a matter of time before we can fight the coronavirus. In scientific research, three months is the equivalent of seconds, and they have been well spent knowing our enemy. Now it’s time to fight it, and in the next news, get over it.
DON’T NECK IT:
- The flu is not a type of coronavirus, its symptoms and its “functioning” are different, so the same treatments and previous knowledge do not work.
- The coronavirus that we are fighting is capable of infecting and being asymptomatic. These patients do not express any symptoms and yet they continue to infect other people with close contact. For this reason, isolation and quarantine are recommended as effective measures. It depends on everyone that this pandemic ends soon.
- Cascella, Marco, et al. “Features, Evaluation and Treatment Coronavirus (COVID-19).” StatPearls, StatPearls Publishing, 2020,
- Perlman, Stanley, and Jason Netland. “Coronaviruses Post-SARS: Update on Replication and Pathogenesis.” Nature Reviews. Microbiology, vol. 7, no. 6, June 2009, pp. 439–50
- Zhou, Peng, et al. “Bat Severe Acute Respiratory Syndrome-like Coronavirus ORF3b Homologues Display Different Interferon Antagonist Activities.” Journal of General Virology, vol. 93, no. 2, Microbiology Society, Feb. 2012, pp. 275–81