The long COVID model attributes to excessive cytokine production, and genetic predispositions

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Excessive production of proinflammatory cytokines may lead to prolonged COVID symptoms due to a genetic predisposition toward not being able to completely clear the virus, according to a review published in Allergy and Asthma procedures.

This model can be used to improve Diagnostic and therapeutic proceduresAnd the Danilo Ponsenso, MD, subordinate The Department of Women’s, Children’s and Public Health at the Fondazione Policlinico Universitaro A. Gemelli Istituti di Ricovero e Cura a Carattere Scientifico in Rome, and colleagues wrote.

Woman having trouble breathing
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Long-term effects of COVID-19

Researchers reviewed the long literature on COVID published in public databases between 2019 and 2022, identifying More than 50 long-term effects from SARS-CoV-2 infection.

The most common effect was fatigue. Shortness of breath, cough, joint and chest pain, as well as problems with thinking, difficulty concentrating, forgetfulness, depression, muscle aches, headache, rapid heartbeat, and fever have also been reported.

These symptoms can persist from weeks to months after COVID-19, according to the researchers, with up to 30% of patients experiencing at least one symptom and long-term effects after 3 months. The infection rate ranged from 10% to 87% of coronavirus cases.

There was a strong female prevalence which, according to the researchers, may be due to increased production of type 1 interferon among women with viral infection compared to men, which may benefit women early in the infection but later lead to a more common harmful inflammatory condition. Corona virus for a long time.

The researchers also noted more than five early symptoms among the risk factors for the coronavirus, including early shortness of breath, prior mental disorders, and specific biomarkers. Researchers have also linked increased body mass index, asthma, and advanced age to persistent inflammation.

Hypothesis model of viral persistence

According to the hypothesis-driven model developed by the researchers, rather than a typical immune response, some patients experience a dysfunctional response in which persistence of the virus leads to an excessive release of proinflammatory cytokines in a phenomenon known as a cellular storm, causing both local and systemic tissue disruption. infection. This failure to eradicate the pathogen followed by its persistence has immunopathological consequences for chronic microbial infection and prolonged COVID pathogenesis.

The researchers wrote that when the virus evades the immune system response, it continues to stimulate the innate and adaptive immune systems, producing harmful expressions responsible for the prolonged development of COVID.

This inflammation and immune dysregulation are associated with diffuse endothelial damage and microcoagulation as organ damage continues, the researchers added. Damage to specific cortical structures can alter taste and smell. Persistent myocarditis can lead to arrhythmias and other heart problems, too.

Among children, neuroinflammatory processes related to lymphoproliferative responses and the subsequent toxic accumulation of inflammatory cytokines in the central nervous system may be associated with neuropsychiatric symptoms.

The researchers also found that gut dysbacteriosis could have a pathogenic role given the relationships between the gut-brain axis in controlling inflammatory conditions in the central nervous system.

Researchers found that more than half of patients with prolonged COVID-19 had reactivation of latent Epstein-Barr virus infection, which has been associated with skin, cardiovascular, hematological and neurological complications that may also occur with prolonged COVID.

The researchers added that the inflammation caused by the persistence of the virus can lead to a long-term infection with Covid disease through long-term damage to the lungs, brain, kidneys and heart in adults and children as well.

According to the researchers, diets lacking in anti-inflammatory substances and/or antioxidants that have potential immune-modulating and antiviral activity could also play a role in developing long-term symptoms after the acute phase of COVID-19.

Finally, the authors cited the role of nuclear factor kappa B and p38, the mitogen-activated protein kinase signaling pathways, which regulate cytokine production, in causing uncontrolled inflammatory responses, acute respiratory symptoms and many prolonged COVID manifestations. The researchers write that understanding these signaling mechanisms will be critical for new diagnostic and therapeutic procedures.