In Research

Why is the SARS-CoV-2 coronavirus, which causes the Covid-19 illness, so efficient and, therefore, so infectious? Since the explosion of the pandemic, scientists all over the world have been searching for answers to this question, which is also essential for finding a cure. David Cyranoski’s article from Shanghai, a correspondent for the scientific journal Nature, is shedding new light on the mechanisms that enable the virus to penetrate different areas of the human body more easily than other types of coronavirus. What are these mechanisms?

First of all, SARS-CoV-2, unlike its closest “relatives”, is capable of attacking several points of the cells and, once it gets inside them, has a very diverse repertoire of harmful molecules. Furthermore, according to Cyranoski, this virus has very sophisticated systems for correcting the errors that occur when its genetic code is duplicated. In this way SARS-CoV-2 does not accumulate mutations that could weaken it. This is perhaps one of the reasons why several antiviral drugs, like ribavirin, used to combat viruses such as hepatitis C, are unable to subdue SARS-CoV-2. Ribavirin, in fact, weakens viruses by inducing a series of mutations, but in SARS-CoV-2, the correction systems cancel out its effects.

It is known that the different types of coronavirus mainly cause respiratory infections (from the common cold to Covid-19). But those that cause colds stop at the upper respiratory tract, whereas those that trigger MERS (Middle East Respiratory Syndrome) and SARS (Severe Acute Respiratory Syndrome) are at ease in the lungs and sometimes, but rarely, in the throat. SARS-CoV-2, on the other hand, can do both, i.e. infect the nose and the throat, but also the lungs directly, with great ease. These two doors give it an advantage and explain why it is highly infectious: SARS-CoV-2 can shed viral particles from the throat into saliva before the symptoms of the disease appear, and these viral particles are easily transmitted from person to person. The SARS-CoV virus, responsible for SARS, is much less effective at doing so and is transferred from one person to the other only when the symptoms are very clear. This in fact helped to contain it.

When SARS-CoV-2 reaches the throat, or the lungs, it latches on to a cell receptor called ACE2 and literally cuts off a little trait of its “spikes” to merge with the cell wall. And then it adds its viral genetic code to the cell, which is duplicated using the host’s cellular “machinery”. In doing so, SARS-CoV-2 demonstrates the extent of what it can do, because it is 10 to 20 times more likely to be able to bind ACE2 than is SARS-CoV. What is more troubling though is that it uses (or at least appears to use) a cell enzyme, called furin, to cut the viral spike protein. This worries researchers, because furin is abundant in the respiratory tract and found throughout the body. To have an idea, furin is the enzyme that is also used by Ebola and the HIV virus.