A new study from Tel Aviv University shows that the many variants of SARS-CoV-2 are likely to develop in chronic COVID-19 patients suffering from immunosuppression. The researchers suggest that a weakened antiframe response, especially in the lower respiratory tract of those chronic patients, may save you a complete cure of the virus and cause the virus to mutate several times during a prolonged infection. In other words, the researchers explain that the ability of the virus to reproduce without restrictions in the framework of the immunocompromised patient leads to the evolution of many variants. In addition, the variants discovered among other chronically ill people with COVID-19 bring many of the same mutations in their evolution as those that occur in variants of fear of serious diseases, namely mutations related to the avoidance of disease-killing antibodies. The new findings imply that while rapidly spreading variants are rare among the many strains transmitted through immunocompromised patients, the likelihood increases and occurs when overall infection rates increase.
The study was led by Professor Adi Stern and PhD student Sheri Harari from the Shmunis School of Biomedicine and Cancer Research at Tel Aviv University’s Wise Faculty of Life Sciences, in collaboration with Dr. Yael Paran and Dr. Suzy Meijer of Tel Aviv Sourasky Medical Center (Ichilov). It was published in the prestigious journal Nature Medicine (Drivers of adaptive evolution Chronic SARS-CoV-2 infections).
Professor Stern explains that since the COVID-19 outbreak, the speed at which the virus evolves is confusing. In the first year of the pandemic, a relatively slow but steady replacement rate was observed. However, since the end of 2020, the global has witnessed the emergence of variants that are characterized by a giant number of mutations, far exceeding the rate observed in the first year. Several clinical hypotheses have emerged about the link between patients with chronic COVID-19 and the rate of mutation accumulation, but nothing definitive has yet been demonstrated. In this new study, Professor Stern and the team shed light on some pieces of this complex puzzle and tried to answer the question of variant formation.
Professor Stern explains: “The coronavirus is characterised because in each population there are other people who are chronically infected. In the case of those patients, the virus remains in their frame for a long time and they have a higher threat. “of recurrent infection. In all the cases observed so far, these were immunocompromised patients: a component of their immune formula is broken and cannot function. In terms of biological evolution, these patients are an “incubator” of viruses and mutations: the virus persists in its frame for a long time and manages to adapt to the immune formula, accumulating mutations.
The study concerned an examination of patients with chronic COVID-19 at Tel Aviv’s Sourasky Medical Center (Ichilov Hospital). According to Professor Stern, the effects reveal a complex picture; on the one hand, no direct link has been discovered between drug treatment against COVID-19 and the progression of variants. On the other hand, the researchers found that it is most likely the weakened immune formula of immunocompromised patients that creates tension for the virus to mutate. In fact, the researchers found that there were chronic patients who had an obvious healing pattern, followed by a recurrent viral infection. In all of those patients, a mutated form of the virus appeared, suggesting that no cure had been achieved; this is partly reminiscent of the modus operandi of HIV after insufficient drug treatment.
After further examination of some patients, the researchers found that when such an obvious recovery trend (based on negative nasopharyngeal swabs) is observed, the virus continues to grow in patients’ lungs. The researchers recommend that the virus accumulate mutations in the lungs and then cross the upper respiratory tract again.
Professor Stern concludes: “The complexity of the evolution of coronaviruses is still being revealed, and this poses many challenging situations for the clinical community. I believe that our studies have succeeded in a missing layer of the big picture and have opened the door to new study efforts to uncover the origins of the other variants. This study highlights the importance of protecting immunosuppressed people, who are at greatest risk of contracting the virus, but who may also be an incubator for the formation of the next variant, which It represents a threat to all of us.
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