The virus hurts less but has not become better, what can be said with certainty



There is currently no evidence of the mutation that would have made the attacker less dangerous. In addition to the indisputable effects of the lockdown, some of the encouraging numbers can be explained by the lesser charge in circulation

by Nicola Barone

Coronavirus: contagion in your region. Molise outbreak

There is currently no evidence of the mutation that would have made the attacker less dangerous. In addition to the indisputable effects of the lockdown, some of the encouraging numbers can be explained by the lesser charge in circulation

5 ‘of reading

Intensive care is emptied. Hand in hand with the diminished pressure on the wards, cases of contagion, new or “old”, despite the progressive overcoming of the lockdown, are down. A picture that unites everyone in relief brings with it the rekindling of the conflict between different medical and scientific perspectives. According to Alberto Zangrillo of San Raffaele in Milan, the new coronavirus “no longer exists clinically” and therefore “terrorizing the country is something for which someone must take responsibility”. By the health authorities the judgment is paid with “absolute bewilderment”, textual words of the President of the Superior Health Council Franco Locatelli. The matter is complex and constantly evolving, however something can be said with probable certainty.

The mutation of the attacker
As far as we know, there are currently no genetic variants of the virus in circulation with greater or lesser virulence (ability to transmit) or pathogenicity (ability to induce disease). This does not of course exclude that such variants can develop. “Viral genome sequencing studies done around the world have identified hundreds of mutations in SARS-CoV-2. But this is no wonder. Viruses change, that’s what they do. The really important question is to understand what kind of benefit these mutations bring to the virus and why they are selected and spread. But no one has yet established with certainty how these point changes in the sequence of viral genes impact the functionality of the virus and the severity of the disease in humans, “explains scientist Ennio Tasciotti specializing in molecular medicine. At the time of the explosion of deaths in Italy the news circulated that the virus had developed more aggressive and contagious forms, partly supported by reports from Chinese scholars according to which L (more aggressive) and S (less aggressive) strains exist, fact not confirmed then through rigorous studies. The point is which of these mutations actually does anything to change the severity or infectivity of the disease. “To date, the only published studies have shown how certain mutations make the virus replicatively more active, more aggressive, or more resistant to certain antiviral drugs. It may be possible that some new mutations lead to a lower replicated capacity of the virus but to date no scientific papers have been published that demonstrate this hypothesis in an incontrovertible way ».

The minor viral load
Beyond the objective and easily detectable drop in the current impact of the disease, on which nobody doubts, the work of Massimo Clementi, director of the Microbiology and Virology Laboratory of San Raffaele, is at the basis of Zangrillo’s thesis. According to the research that will be published shortly between March and May, the amount of virus present in positive subjects has decreased by very, very much. “A study published today in Lancet on 70 patients shows that the average viral load of severe cases was about 60 times higher than that of mild cases, suggesting that higher viral loads could be associated with serious clinical outcomes. To understand whether the initial dose of SARS-CoV-2 is related to the severity of the symptoms, studies should be done in which the virus is inoculated to healthy volunteers in order to study how the disease evolves and how the patient responds. These studies are ethically questionable because of the potential severity of the disease and therefore this question can only be answered indirectly by observing similar studies carried out on other viruses, “says Tasciotti. “A 2015 study using the H1N1 influenza virus injected into healthy volunteers showed that there is an optimal charge of viruses capable of triggering the infection and that below that threshold the severity of the disease and the ability to isolate viruses from the mucous membranes- pharyngeal decreases. Since coronavirus is also a respiratory virus and that the same tissues are exposed in this type of infections, similar conclusions can also be drawn for SARS-CoV-2 “.

The type of infected subject
Turning to the field of hypotheses that could explain the macroscopically more favorable trend of the numbers, it is that in recent weeks the majority of cases of new infection have affected people less at risk for serious complications or by age group or associated comorbidities. «The amount of virus that comes into contact with the body is only part of the story. The other fundamental component of this equation is how the body responds to the virus. We learned that if the immune system is not activated, viral replication proceeds uncontrollably. This happens for all elderly patients, those who are immunocompromised or immunocompromised such as cancer patients. On the other hand, if the immune system is hyperactivated, it ends up damaging the tissues and creating severe symptoms. This could happen in patients with other concomitant inflammatory diseases (diabetes and cardiovascular) “. On this point, the scientist, long in the United States and very active on the dissemination of Covid-19 even for non-experts, leaves the door open. “A further hypothesis therefore remains, namely that the patients we observe today no longer belong to these classes, who were the first to suffer from the effects of the first wave of infections. The more fragile classes have maintained a more ironic distancing and other precautions and have therefore protected themselves while those we see today are the patients who were a priori less weak and who have an immune system capable of responding to and inactivating the virus. Fewer viruses in the body means less severe symptoms but also fewer viruses in the mucous membranes that are tested with the rhino-pharyngeal swab and this could explain why we are recording different values ​​at this stage of the epidemic ».

Role of mucosal immunity
Finally, a suggestion on which the attention of some researchers is focusing and which Tasciotti is keen to highlight. The different climatic conditions and the attendance of open spaces facilitate the rapid evaporation and dispersion of the droplets and consequently the inactivation of the virus charge. «The smaller quantities of viruses may not be sufficient to penetrate the body up to the deep pulmonary alveoli where the viruses cause more serious symptoms but stop at the level of the upper respiratory tract. At that level there is an additional type of immune defense which has not been talked about much but which is just as important as the humoral one that is measured by serological tests (IgM and IgG). This innate mucosal immunity is mediated by the secretion of a different class of antibodies, called type a immunoglobulins (IgA). Studies with other human variants of coronavirus have shown that the presence of IgA was associated with reduced risk of infection, seroconversion and symptomatic disease. These HCoV studies indicate that mucosal immune responses (mucous IgA) provide possible correlates of protection from infection and disease. “

Source link


Please enter your comment!
Please enter your name here