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Covid: the cold blocks the virus (but for a short time)

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Sars-CoV-2 has a new, unsuspected, enemy: the common cold. According to a study by the University of Glasgow, in fact, the rhinovirus which causes colds, thanks to the immune response it causes when it infects us, can prevent Sars-CoV-2 replication. Although this effect, the study suggests, is temporary. The scientific field of virus-virus interactions is not yet much explored, but something is known: for example that while some viruses, such as adenoviruses, can coexist peacefully with other viruses, there are also more competitive viruses, such as the seasonal flu, which minimize the possibility of other competing infections.

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“This study on Sars-CoV-2 and colds is the continuation of a study we published in December 2019, in which we showed that respiratory viruses interact with each other – he explains. Pablo Murcia, Professor of Virology at the University of Glasgow, interviewed by Salute – the most interesting observation from that study is that when there is a high prevalence of rhinoviruses in the population, then there is a low prevalence of influenza. And viceversa. This both at the epidemiological level and at the level of the individual patient “.

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After the onset of the pandemic, Murcia wondered how Sars-CoV-2 interacted with other respiratory viruses. “The best candidate to study was the human cold rhinovirus (HRV), because we knew it negatively interacts with the flu virus, and also because it is the most common human respiratory virus – he explains – the only problem was that we couldn’t study. this interaction between viruses from an epidemiological point of view: with all the anti-Covid measures taken – social distancing, masks, lockdowns – the transmission of respiratory viruses has been greatly reduced and this would therefore have distorted the results “.

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That’s why Murcia decided to test his hypothesis in the laboratory, injecting Sars-CoV-2 and the cold rhinovirus into cultures of human bronchial epithelial cells, to see how they replicate. “We have seen that the rhinovirus replicates both in the absence and in the presence of the coronavirus. But the really exciting thing was to discover that Sars-CoV-2 cannot replicate in the presence of the rhinovirus – explains Murcia – we have seen that even if you give at Sars-CoV-2 a 24-hour advantage, when you inject HRV, Sars-CoV-2 is strongly inhibited in its ability to replicate. “

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How can this result be explained? “What we have observed is that what blocks Sars-CoV-2’s ability to replicate in infected cells is the interferon-mediated immune response to HRV. This is part of the innate immune response that cells activate when they are invaded. from a virus – explains Murcia – it is important to add, however, that this innate immune response is short-term, transient: the effect of substantial immunization to Sars-CoV-2 lasts no more than a few days “.

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To further investigate this virus-killing effect, the next step for the Glasgow group was a population-level study. “In the absence of epidemiological data, in collaboration with Imperial College London, we carried out computer simulations using realistic models of the spread of the virus – explains Murcia – and what the models suggest is that when there is a high prevalence of rhinovirus, there will be a decrease in the number of new cases of Sars-CoV-2 infection. So the effect that is seen at the level of the single organism can also translate into an effect on the population “.

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The practical consequence of the new study is not an anti-Covid therapy based on colds, but an aid to the ability to plan resources – such as hospital places and doses of the vaccine – useful for fighting the pandemic: “If in a certain period we has a strong incidence of influenza viruses or human rhinovirus, health authorities can expect a reduction in Sars-CoV-2 infections – concludes Murcia – and allocate resources accordingly “.

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