Scientists from Israel found a type of patients more likely to generate mutations in their body, which are then transmitted. Research paves way for better understanding of new strains
Source: Infobae
A series of virus specialists from Tel Aviv University (TAU) and the Sourasky Medical Center, both in Israel, have discovered the answers and have just published them in the journal Nature. The study was led by Adi Stern and doctoral student Sheri Harari of the Shmunis School of Biomedicine and Cancer Research in TAU’s Wise College of Life Sciences, in collaboration with Yael Paran and Suzy Meijer of Sourasky Medical Center.
Among their conclusions, they revealed that patients with weakened immune systems due to chronic diseases and those who take medications that reduce the body’s ability to fight invading pathogens are at risk of chronic infection and develop several highly mutated coronavirus variants.
Although this is puzzling, they also provided some good news: While many different variants form in immunocompromised patients, these mutated forms are less likely to spread to others.
COVID-19 infections typically end within a few days, the same as RNA shedding, but a growing number of case reports are accumulating documenting chronic infections spanning weeks to many months of infection.
“In particular, chronic infection should not be confused with prolonged COVID, where the infection clears quickly but symptoms persist; in cases of chronic infections, a replicative virus is detected for long periods”, the specialists wrote in their document.
The researchers suggest that a weakened antibody response, especially in the lower respiratory tract of these immunosuppressed patients, may prevent full recovery and cause the virus to mutate many times during prolonged infection. As a result, the ability of the virus to survive and reproduce in the bodies of these patients without restriction leads to the evolution of many variants.
The scientists also found that variants found among chronically ill patients with COVID-19 have many of the same mutations in their evolution as those present in variants that have the potential to cause severe disease, particularly those mutations associated with antibodies. elusive that kill diseases.
The new findings indicate that while fast-spreading variants are rare among the many strains emanating from immunosuppressed patients, the likelihood increases and they emerge when global infection rates rise.
Stern noted that “since the COVID-19 outbreak, the speed at which the virus has evolved has been quite puzzling. During the first year of the pandemic, a relatively slow but steady mutation rate was observed, but since the end of 2020, the world has seen the emergence of variants that are characterized by a large number of mutations, many more than in 2019.”
Since then, researchers have suggested various scientific hypotheses about the link between chronic COVID-19 patients and the rate of mutation accumulation, but nothing definitive has yet been proven. In this new study, the team shed light on some pieces of this complex puzzle and tried to answer the question of how variants are formed.
“The coronavirus is characterized by the fact that in each population there are people who are chronically infected. In these cases, the virus remains in the bodies for a long time and they have a high risk of recurrent infection. In all the cases observed so far, they were immunocompromised patients: part of their immune system is damaged and cannot function. In terms of biological evolution, these patients constitute an incubator for viruses and mutations: the disease persists in their body for a long time and manages to adapt to the immune system by accumulating various mutations”, explained Stern.
The study involved an examination of chronic COVID-19 patients at Ichilov de Sourasky Hospital. The results revealed a complex picture: on the one hand, no direct connection was found between treatment with anti-COVID-19 drugs and the development of variants.
But on the other hand, the team found that the weakened immune system of immunocompromised patients likely creates pressure for the virus to mutate. In fact, the researchers found that there were chronic patients who showed a pattern of apparent recovery, followed by recurrent viral infection. In all of these patients, a mutated form of the virus emerged, suggesting that they had not actually recovered. This is partially similar to the way the AIDS virus, HIV, operates when the patient has not taken the proper antiretroviral drugs.
Upon closer examination of some patients, the researchers found that when a pattern of apparent recovery is observed (based on nose and throat swabs that tested negative for the disease), the virus continues to thrive in the lungs. The researchers therefore suggested that the virus accumulates mutations in the lungs and then travels back to the upper respiratory tract.
“The complexity of the evolution of the coronavirus is still being revealed, and this poses many challenges to the scientific community. I believe that our research has succeeded in removing a missing layer of the big picture and has opened the door for more research efforts to uncover the origins of the various variants. Our study highlights the importance of protecting immunocompromised people who are at high risk of contracting the virus and also recognizing that they may be an incubator for the formation of the next variant and pose a risk to all of us.”
