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Covid-19, a study reveals the origin of the new variants

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Covid-19, a study reveals the origin of the new variants

A new study from Tel Aviv University (TAU) reveals that many variants of SARS-CoV-2 are likely to form in chronic COVID-19 patients suffering from immunosuppression. Researchers suggest that a weakened antibody response, particularly in the lower airways of these chronic patients, can prevent full recovery from the virus and cause the virus to mutate many times during a long infection. The new results indicate that fast-spreading variants are rare among the many strains originating from immunosuppressed patients, but occur when overall infection rates rise. The study was conducted by Professor Adi Stern and Ph.D., student Sheri Harari of the Shmunis School of Biomedicine and Cancer Research at TAU’s Wise Faculty of Life Sciences, in collaboration with Dr. Yael Paran and Dr. Suzy Meijer of Tel Aviv Sourasky Medical Center (Ichilov). The study was published in the pages of the journal Nature Medicine.

Professor Stern explains that the The speed at which the virus evolves has been somewhat staggering since the outbreak of COVID-19. During the first year of the pandemic, a relatively slow but constant rate of mutations was observed. However, since the end of 2020, the world has seen the emergence of variants characterized by a large number of mutations, which far exceed the rate observed during the first year. Various scientific hypotheses have emerged about the link between chronic COVID-19 patients and the rate of accumulation of mutations, but nothing definitive has been shown. In this new study, Stern and his team shed light on some pieces of this complex puzzle and try to answer the question of how variants are formed.

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“The coronavirus is characterized by the fact that, in every population, there are people who become chronically infected – explains the expert -. In the case of these patients, the virus remains in their body for a long period of time and they are at high risk for recurrent infections. In all cases observed so far, they were immunocompromised patients: part of their immune system is damaged and unable to function. In terms of biological evolution, these patients constitute an ‘incubator’ for viruses and mutations: the virus persists in their body for a long time and manages to adapt to the immune system by accumulating various mutations”.

The study involved an examination of chronic COVID-19 patients at the Tel Aviv Sourasky Medical Center (Ichilov). The results reveal a complex picture: on the one hand, no direct connection was found between anti-COVID-19 drug treatment and the development of variants. On the other hand, research has found that it is probably the weakened immune system of immunocompromised patients that creates pressure for the virus to mutate.

In fact, the researchers found that there were chronic patients who exhibited a pattern of apparent recovery, followed by a recurring viral infection. A mutated form of the virus emerged in all of these patients, suggesting that healing had not been achieved; this is partly reminiscent of the modus operandi of HIV following inadequate pharmacological treatment.

Upon closer inspection of some patients, the researchers have found that when such a pattern of apparent recovery is observed (based on negative nasopharyngeal swabs), the virus continues to thrive in patients’ lungs. Researchers suggest that the virus accumulates mutations in the lungs, then returns to the upper respiratory tract.

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“The complexity of the evolution of the coronavirus is still being revealed and this poses many challenges to the scientific community – concludes Professor Stern -. I believe our research has managed to remove a missing layer of the big picture and has it opened the door to further research efforts to uncover the origins of the variants. This study underlines the importance of protecting immunocompromised individuals, who are at high risk for the virus, but can also be an incubator for the formation of the next variant, putting us all at risk. “

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