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Italy, Spain, France, Japan. The English variant is no longer English only – new cases are emerging around the world. According to some experts, we will have to get used to the drips of the virus. Especially with the spread of vaccines. “Herd immunity and vaccine-induced immunity, as well as antiviral therapies or other strategies could exert selective pressure and push the virus to survive and escape,” he writes for example Ralph baric, virologist at the University of North Carolina, sul New England Journal of Medicine. “This selective pressure,” asks the expert, “will it increase the spread of the virus, modify the severity of the disease, or will it push Sars-Cov-2 to become extinct or go to other host species?”
That is, will the vaccine push the virus to evolve to escape our strategies? This is similar to what happens with antibiotics, the use of which can cause resistant strains of bacteria to develop. “I like to quote Lucio Battisti, we will only know it by living,” he replies. Fausto Baldanti, head of the San Matteo molecular virology laboratory and professor at the University of Pavia. “We are used to associating something bad with the word mutation. In reality we are facing an adaptation process. As a virus evolves, in general, a virus learns not to kill its host. Its interest is to spread, not harm.” The immune system, alone, is capable of putting the coronavirus under pressure. Even without a vaccine. “Our body is a hostile ecosystem, our defenses react very strongly. We see it in the large number of infected people with mild symptoms.”
“When drugs are used against a virus, he explains Andrea Cossarizza, an immunologist at the University of Modena and Reggio Emilia, it may happen that a mutation alters the site where the drug binds and, therefore, cancels its effectiveness. All viruses sensitive to this drug no longer replicate, except for the mutated one, which becomes dominant. We have seen it many times with HIV, but today we have many medications available to treat this infection. ”
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The appearance of strains resistant to treatments and vaccines, therefore, is not a remote hypothesis. “It happens when we are faced with imperfect vaccines,” he explains. Luca ferretti, researcher in Statistical Genetics and Pathogen Dynamics at the University of Oxford. Ferretti cites the case (involving only chickens) of the Marek virus. “It is dangerous because it induces tumors. Vaccines are effective in preventing tumors, but not so effective in stopping infections. The result has been the selection over time of a more virulent strain.”
The parallel with our Covid vaccines, effective in mitigating symptoms but not necessarily preventing infections, is evident. “If phenomena of resistance to the vaccine were to occur – continues Ferretti – we should be good and find out in time. Reprogramming new and modern vaccines such as Covid, especially if they are RNA, will not be especially difficult or long.
The chances of making a winning dribble with a mutation, for the coronavirus, increase with a high number of infections. “In Australia, where there are few cases, a variant possibly born after a vaccination campaign would have less chance of taking hold,” explains Ferretti. “In the case of a rampant epidemic, on the other hand, mutations are more likely to spread.” In any case, Sars-Cov-2 is not expected to turn into a chameleon, like the flu. “Unlike the flu – explains Baldanti – the coronavirus has a proofreading system that cancels out mutations when, in each replication of the genome, they occur randomly. This reduces variability, even if it cannot completely eliminate it. ” .
In addition to the English mutation, in recent times another has been noticed in South Africa, even earlier in Spain. We were previously familiar with D614G, which actually made the coronavirus more contagious. “We have also observed slightly different viruses between Lodi and Bergamo,” said Baldanti, who published the data in Nature Communications. “And we saw what differences there were, in the intensity of the epidemic, between the two cities.” Also in the Pavia laboratory tonight two cases of “English variant” were identified in two travelers who landed on December 23 and 24 in Milan Malpensa.
Other mutations, adds Cossarizza, “have been described in many other parts of the world, from Denmark to Australia to South Africa, and have been present for some time in international databases that count hundreds of thousands of sequences.” In the case of the English variant, the researchers suggest that therapies such as convalescent plasma or remdesivir may have put “pressure” on the virus genome, causing it to mutate. “I don’t think – Cossarizza is skeptical – that this is the cause. These are poorly effective therapeutic approaches.”
The arrival of more vaccines, their combination with drugs such as monoclonal antibodies, the slow development of herd immunity among those recovered, according to Baldanti (who will be vaccinated tomorrow) are still good news. The virus will try to find a way out between these barriers. “But the weapons we have at our disposal are many, and the research is to be thanked for that. Because the daily battles against the coronavirus take place in the hospital. But it is in the laboratory, with the help of science, where they are won the wars”.
Incoming vaccines, explains the virologist, have the advantage of stimulating both antibodies (the proteins that neutralize the virus and prevent it from entering our cells), and T cells, responsible for killing infected cells that are dedicated to making new ones. virus particles. “Although changed, it is difficult for the virus to escape this double attack,” explains Baldanti. “In any case, we have all the tools to control what will happen. We are researchers. We do not have dogmatic certainties.”
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Cossarizza shares the optimism: “We cannot know what will happen in the future, but I would be quiet enough. Vaccines induce a polyclonal immune response. It means that many lymphocytes are formed that produce antibodies against different portions of the coronavirus peak protein. Mutation could (but we are always in the field of assumptions) decrease the effectiveness of one of the hundreds of different antibodies capable of intercepting and blocking the virus. But experience teaches us that To escape the immune response, a virus must accumulate a large number of mutations, and it takes many years to do so. Monoclonal antibodies, whose use could be very important in the early stages of infection, have been designed to recognize highly conserved portions of the virus. “
One of the unknowns is still our social habits. Clubs yesterday and Christmas shopping today are part of those variables that make the behavior of a virus unpredictable. “I remember the Ebola era,” says Ferretti. “Many of our experts continued to wonder why the inhabitants of the affected African countries continued to hug their dead, since that was a source of contagion. Today we see how much effort it takes to stop eating together or doing Christmas shopping ”. Winning viruses use receptors to enter our cells. But they also find the right keys to insinuate themselves between our habits and our psychology.
What seems certain, among so many mutations, is that the Sars-Cov-2 genome is still in motion. The address is the most contagious, although the announcement of the most affected children remains to be verified. “We have seen an increase in cases between the ages of 10 and 19,” explains Ferretti. “But we are not sure if the mutation is the cause.” In Britain during this period, schools remained open despite the closure.
The arrival of vaccines could accelerate the evolution of the coronavirus, but according to Baldanti it will not change the course of the war. “We live with four other coronaviruses that give us a cold and who knows, maybe in the past they were as terrible as this pandemic. With Sars-Cov-2 we may be witnessing the birth of the fifth cold ”. In short, neither he nor we will win. “A truce is more likely to come.”
In any case, says Cossarizza, “we must hurry to vaccinate everyone, everywhere. The chess game between us and the virus will not be short. We have moved the pieces for a few seconds, so we have black, and for now We are not in the conditions to give the coronavirus checkmate in two plays. But I am convinced that we have the ability to become masters, eat one opponent’s piece after another, and take home the checkmate. “
