After SARS in 2003 and MERS in 2012, a new coronavirus, dubbed 2019-nCoV, is of concern to international health authorities. A cousin of SARS and probably a descendant of a bat virus, it is said to have emerged at the beginning of last December in Wuhan, China.
As of January 30, 2020, 7,891 infections have been confirmed in twenty countries, causing 170 deaths, only on Chinese soil so far. What caused these deaths? How do coronaviruses make us sick? Are there predispositions to these infections?
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On the medical level, there are two groups of coronaviruses: low pathogenic coronaviruses (there are currently four), and highly pathogenic coronaviruses, of which only two representatives are known at the moment, SARS-CoV (for severe acute respiratory syndrome – severe acute respiratory syndrome or SARS in French) and MERS-CoV.
For the moment, the available data are too incomplete to allow to affirm that the virus which emerged in Wuhan belongs to one or the other of these categories. We will have to wait for more information, especially from the Chinese health authorities.
Low pathogenic coronaviruses circulate in France every year in the fall, throughout the winter and in the spring, but disappear during the summer. For these viruses as for the other seasonal viruses (flu, colds, gastroenteritis…), the reasons for this summer break are poorly understood.
Being confined to buildings in winter is likely to facilitate the transmission of viruses. What’s more, weather conditions certainly play a role. No precise mechanism has yet been identified, but we know for example that certain viruses such as the flu seem to resist hot airless well than cold and dry air. In addition, the latter weakens the nasal mucosa, facilitating the penetration of respiratory viruses such as coronaviruses.
When a person infected with coronavirus sneezes, droplets of nasal secretions loaded with viral particles are projected around him, the finest (aerosols) traveling further than the largest. For the moment, it is not known if 2019-nCoV is transmitted by aerosol or if only the largest droplets are infectious. However, it appears to be better transmitted than SARS or MERS-CoV, which, surprisingly, has not spread beyond the Arabian Peninsula.
If a healthy person gets splashed and breathes droplets containing coronaviruses, a new infection begins. Initially, the viruses penetrate into the nasal cells thanks to a protein “key”: protein S (from the English Spike, “tip, ear”). Present in numerous copies on the surface of the virus, it gives it the “crown” aspect to which it owes its name, coronavirus.
This “key” interacts with a “lock” located on the surface of human cells, allowing the virus to cling to it and then enter it. Not all coronaviruses have the same types of keys, and therefore do not recognize the same locks. On the other hand, said locks being essential to the functioning of our organism, we have them all in us. We are therefore all likely to be infected with coronaviruses.
Once inside a cell, the coronavirus pirates it and forces it to make a large number of copies of itself. After a relatively short time, 6 or 8 hours later, these copies leave the infected cell (usually by destroying it) and go to attack its neighbors.
If the infection is due to a pathogenic coronavirus, the symptoms for a healthy person are usually those of a cold.
The problem is that the locks that allow coronaviruses to enter airway cells are also present on cells in other organs, such as the kidneys or intestines. Coronaviruses can therefore also infect them. In this, coronaviruses differ from influenza viruses, which recognize only structures present on cells of the respiratory system. This explains why the flu does not give a kidney or intestinal signs.
In the case of highly pathogenic viruses such as MERS or SARS, the affected organs can be severely damaged. In addition to severe lung failures, which lead to respiratory distress, patients are sometimes victims of kidney failure (which will require dialysis), heart failure, etc. Unfortunately, transfer to intensive care is not always enough, and some people die.
The knowledge accumulated following the epidemics due to SARS and MERS has made it possible to better understand the factors which influence the outcome of the infection. The relationship between the coronavirus and the patient’s immune system is particularly important.
The elderly and immunocompromised are most at risk
We know that the people most prone to complications are those who are immunocompromised (due to illness or medical treatment) or whose immune system works less well, like that of the elderly. The virus takes advantage of these failures and replicates better.
A few years ago, a patient undergoing immunosuppressive treatment due to transplantation, for example, died from an infection with MERS-CoV. Muzzled to prevent him from rejecting the transplant, his immune system could not contain the viral infection, which had generalized, reaching all the organs.
Conversely, young people, whose immune systems are very efficient, are generally less affected. Thus, for MERS-CoV, almost no contamination of children has been described; rather, it is a disease of adults and the elderly.
The situation was different in the case of SARS: its fatality rate was not only higher than that of MERS but also the virus caused the death of young patients.
2019-Nov: a lack of information
The first information concerning the new coronavirus seems to indicate that the deaths concern very old people, who already have other pathologies. The rest of the people appear to be healing fairly quickly, which would explain why there are currently “only” 170 dead out of more than 7,800 officially declared infections.
Information is still lacking, however, and some of the information available seems to differ from the observations made on patients whose disease has started in France. Thus, the first information disseminated by Chinese doctors seemed to indicate the existence of pneumonia, that is to say, a lower lung infection.
However, some of the patients hospitalized in our country do not seem to develop this type of lung tissue damage. In their case, the infection remains in the upper respiratory tract, mainly the nose and probably the throat and sinuses. The situation would, therefore, be different, for example, from infection with MERS: in this case, the virus enters through the nose and descends very quickly in the respiratory tract. In one in two cases it is not found in the nose, while it is already present in the bronchial and pulmonary areas.
The question of healthy carriers also remains to be decided. Given what we know about other coronaviruses, we can assume that some people have an immune system capable of reacting very well to 2019-Nov. These would present mild symptoms, which would not lead them to consult. We don’t go to see our doctor if we just have a runny nose! However, they would be contagious and would spread the epidemic without knowing it.
In order to be able to clarify this essential point, it will be necessary to wait for further information from Chinese doctors.
A virus in the process of adapting to humans
Viruses can mutate. Should we fear that the coronavirus will become more dangerous for humans? Probably not. There is no known case of low pathogenic coronavirus which has become highly pathogenic.
On the contrary, coping mechanisms generally cause highly pathogenic viruses to lose virulence over time. Thus, the viruses responsible for influenza pandemics are initially relatively poorly adapted to humans. Little by little, they accumulate mutations, and they become less pathogenic.
It can be assumed that coronaviruses are also subject to similar mechanisms. In fact, the only known highly pathogenic coronaviruses have emerged very recently: in 2003 for SARS and in 2012 for MERS. Conversely, studies on the genomes of low pathogenic coronaviruses have revealed that they passed into humans several decades ago, probably in the 1940s or 1950s. Unlike SARS and MERS, they, therefore, had time to lose virulence.