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The post-COVID syndrome (long-term covid) is a wide range of long-term symptoms caused by the SARS-CoV-2 virus. The post-COVID syndrome affects almost 3% of the UK population.

For different coronavirus strains, the prevalence and duration of post-COVID syndrome vary. In 51-87% of patients with post-COVID syndrome, symptoms persist after 2-6 months of observation and gradually decrease after 6-12 months.

Scientists at the University of Birmingham in the UK have found out what symptoms accompany the post-COVID syndrome. More than 486,000 coronavirus survivors participated in the study. The control group is almost 2 million healthy people. The criterion for the post-COVID syndrome is persistent symptoms 12 or more weeks after the onset of COVID-19.

Symptoms of the post-COVID syndrome

The most common symptoms are fatigue, shortness of breath, sleep disturbances and cognitive impairment.

Some patients complain of:

  • loss of taste and smell;
  • cough;
  • joint pain;
  • chest pain;
  • headache;
  • hair loss;
  • diarrhea;
  • sneezing;
  • difficulty in ejaculation;
  • decreased libido;
  • hoarse voice;
  • fever.

Cough and shortness of breath may persist for 2-3 months after infection and improve after 6 months. Fatigue and neuropsychiatric symptoms may persist longer. The “brain fog” that patients with post-COVID syndrome complain about can persist for up to 6-12 months.

Symptoms of post-COVID syndrome can be identified by blood plasma proteins

Scientists from the National Heart and Lung Institute in the UK found that certain proteins in blood plasma are associated with specific post-COVID syndrome symptoms. These proteins can serve as biomarkers to detect symptoms and prescribe the most effective treatment. The results of the study:

  • IL-1R2, MATN2, and COLEC12 proteins are elevated in cardiovascular symptoms, fatigue, anxiety, and depression.
  • MATN2, CSF3, and C1QA are elevated in gastrointestinal symptoms.
  • C1QA is elevated in cognitive impairments.
  • DPP10 and SCG3 may be associated with inflammatory bowel diseases and irritable bowel syndrome.
  • NFASC and SPON-1 proteins, regulating neuron growth, may indicate neuroinflammation and potential neurodegenerative processes.

Further study details are available in the article “Blood Markers Associated with Post-COVID Syndrome“, published in the journal Nature Immunology.

How Post-COVID Syndrome Manifests Depend on Gut Microorganisms

The symptoms of post-COVID syndrome depend on the composition and diversity of the gut microbiota. Chinese scientists from the Microbiota Center reported this. Using artificial intelligence, the researchers analyzed the microbiota of more than 1200 individuals with post-COVID syndrome.

Patients with post-COVID syndrome showed reduced diversity and quantity of gut bacteria compared to control groups, who either had COVID-19 without long-term effects or had never contracted the virus. Particularly notable were the decreases in the quantities of Bifidobacterium adolescentis and Roseburia hominis, depletion of Adlercreutzia equolifaciens, Bifidobacterium teenis, and Gemmiger formicilis, as well as an increase in Clostridium bolteae and Flavonifractor plautii.

In 13% of cases, the symptoms of post-COVID syndrome were linked to changes in the microbiota. This correlation was more substantial than those with vaccination status, the severity of the initial COVID-19 infection, and demographic factors.

The prevalence of symptoms based on the dominant type of gut bacteria included:

  • Respiratory symptoms—such as shortness of breath, cough, runny nose, and chest pain—were commonly observed in patients with predominant Ruminococcus gnavus and Clostridium bacteria.
  • Neurological issues—such as memory loss, difficulty concentrating, insomnia, and blurred vision—were more frequent in individuals with predominant Eubacterium rectale and Asaccharobacter celatus.
  • Gastrointestinal problems were associated with a predominance of Coprobacillus cateniformis.
  • Patients with a higher prevalence of bifidobacteria experienced less fatigue than other groups.

Details of the study can be found in the article “Artificial Intelligence Predicts Post-COVID Syndrome by Microbiome.” The research was published in the journal Cell Host & Microbe.

Risk factors for the post-COVID syndrome:

More prone to the post-COVID syndrome are:

  • young;
  • women;
  • less economically secure persons;
  • less socially active persons;
  • smokers;
  • obese and other comorbidities, such as chronic obstructive pulmonary disease.

Causes of The Post-COVID Syndrome

American scientists have shown that one of the causes of the post-COVID syndrome is inflammation that persists after infection with COVID-19. The study involved 24 people who had coronavirus 1-3 months ago. Among them were people with neurological and other complaints about the post-COVID syndrome.

All participants retained inflammation after COVID-19:

  • The level of IL-4, a cytokine essential for brain function, including memory function, was significantly increased. IL-4 counteracts pro-inflammatory cytokines. An increase in IL-4 levels may signal the body’s attempt to suppress neuroinflammation.
  • Participants with neurological symptoms had slightly elevated levels of IL-6, a cytokine associated with the acute phase of inflammation. Chronically elevated levels of IL-6 may predict disability in old age.

Some Post-COVID Syndrome Symptoms Linked to Single and Multi-Organ Failure

Researchers from the United Kingdom have compared the symptoms, blood tests, and magnetic resonance imaging (MRI) data of patients with post-COVID syndrome. Blood tests, on the whole, were regular, except for elevated lactate dehydrogenase, creatine kinase, cholesterol, and average hemoglobin concentration. MRI revealed abnormalities in one organ in 59% of patients and two or more organs in 23%. Typically, the abnormalities were mild, with hepatic steatosis, fibrotic kidney inflammation, and spleen enlargement being the most frequently observed.

Hepatic steatosis was associated with systemic symptoms and severe shortness of breath. Patients with lung impairment and dysfunction of three or more organs experienced the most symptoms.

Changes in liver parameters were associated with Post-COVID Syndrome symptoms:

  • High liver fat levels were present in 31% of patients with severe shortness of breath but only in 21% without severe shortness of breath. Conversely, low liver fat levels were more likely in those without severe shortness of breath.
  • Enlarged livers were linked to a lower quality of life. Liver enlargement was observed in 14% of patients with a lower quality of life but only in 5% with a higher quality of life.

Symptoms, blood test results, and MRI could not predict the progression of post-COVID syndrome or when recovery would occur. Most symptoms resolve within 12 months, especially those related to cardiac and pulmonary systems and systemic issues.

Further study details are available in the article “Post-COVID Syndrome and Multi-Organ Failure,” published in the Journal of the Royal Society of Medicine.

Mechanisms of Post-COVID Syndrome

Reservoirs of Coronavirus Contribute to the Development of Post-COVID Syndrome

Researchers from premier institutions in the United States, Sweden, the United Kingdom, and South Africa conducted extensive patient evaluations who had recovered from COVID-19. The findings revealed that the coronavirus is capable of remaining concealed in various organs for up to 16 months post-recovery, establishing reservoirs of its active genetic material. The virus’s protein presence in the bloodstream is intermittent, emerging predominantly during periods of weakened immunity, which in turn facilitates more vigorous viral replication. This prolonged viral persistence in the body sustains inflammation and contributes to the manifestation of post-COVID syndrome symptoms.

The scientists identified six mechanisms through which viral reservoirs influence the development of post-COVID syndrome:

  1. Excessive immune response and chronic inflammation leading to the depletion of immune cells and immunopathology.
  2. Impairment and death of cells in organs or tissues that serve as reservoirs.
  3. Suppression of innate immunity.
  4. Disruption of natural cellular life processes and gene activity within the body.
  5. Increased blood coagulability and the formation of abnormal pro-inflammatory thrombi containing SARS-CoV-2 spike proteins.
  6. Reactivation of latent infections due to the suppression of the interferon system.

Researchers believe that a key role in the pathogenesis of post-COVID syndrome is played by the disruption of the gut microbiome caused by coronavirus reservoirs. Initially, a changed immune response deteriorates the diversity and activity of the microbiome. Consequently, the microbiome begins to produce metabolites differently, which regulate the body’s immune and humoral systems. Additionally, dysbiosis increases susceptibility to infections due to impaired synthesis of pathogen-neutralizing molecules. Dysbiosis also exacerbates intestinal inflammation and increases its permeability, facilitating pathogen movement and sustaining inflammation.

The scientists emphasize that coronavirus reservoirs also contribute to autoimmune diseases. They link the mechanism of autoimmunity to the chronic form of COVID-19, which stimulates the production of neutralizing autoantibodies by the body. These antibodies react not only to SARS-CoV-2 but also to cells in the heart, intestines, lungs, kidneys, and brain, resulting in organ damage and functional deterioration.

Viral reservoirs can also be a direct cause of various post-COVID syndrome symptoms: fatigue, reduced concentration, muscle and joint pain, sleep disturbances, anxiety, and depression. This mechanism is linked to the vagus nerve, which innervates internal organs and regulates inflammation levels. Branches of the vagus nerve can detect immune responses to SARS-CoV-2 in tissues, leading to neuroinflammation and the onset of post-COVID syndrome symptoms.

Furthermore, coronavirus reservoirs increase the risk of dementia. For instance, the mechanism of post-COVID Alzheimer’s disease is linked to viral damage to the central nervous system. To defend against infections, the brain produces the antimicrobial protein beta-amyloid. However, this protein also heightens the risk of developing Alzheimer’s disease in both the short and long term.

The details of this research are elaborated in the article “Confronting the Invisible Enemy: How Viral Reservoirs Impact Health Post COVID-19,” published in the journal Nature Immunology.

Scientists from the Pasteur Institute in Paris discovered that alveolar macrophages act as viral reservoirs in long COVID and that the persistence of SARS-CoV-2 in these macrophages is regulated by NK cells and IFN-γ. In a study on macaques, replication-competent SARS-CoV-2 remained in alveolar macrophages 18 months post-infection.

The virus altered macrophage function, leading to increased expression of MHC-E, IL-10, and CD11c, as well as genes associated with inflammation (S100A8/S100A9) and NK-cell activation (CD1b). These changes coincided with a reduction in IFN-γ production.

SARS-CoV-2 suppressed NK cells’ ability to produce IFN-γ and control viral replication by interacting with them. When SARS-CoV-2-infected macrophages were cultured with IFN-γ at 100 IU/mL, IFN-γ significantly reduced viral RNA levels. Additionally, higher IFN-γ expression in NK cells correlated with lower levels of the SARS-CoV-2 spike protein in macrophages.

While IFN-γ inhibited viral replication, it simultaneously enhanced macrophage resistance to NK-cell-mediated killing by increasing MHC-E expression in macrophages. MHC-E is a molecule involved in antigen presentation; it binds to the NKG2A receptor on NK cells, suppressing their activity and protecting the infected cell from destruction. Moreover, the V3-11 peptide of the SARS-CoV-2 spike protein interacted with MHC-E, further inhibiting NK-cell activity, representing one of the mechanisms by which the virus evades immune responses.

Restoring NK-cell function and clearing infected macrophages could provide a viable immunotherapeutic strategy for treating long COVID.

The details of the study are presented in the article “Persistence of SARS-CoV-2 in Alveolar Macrophages is Regulated by IFN-γ and NK Cells“, published in Nature Immunology.

Post-COVID Syndrome Associated with Complement Activation

Swiss researchers have uncovered another mechanism underlying the development of post-COVID syndrome: increased activity of the complement system.

The complement system is a part of the immune system comprised of blood proteins that enhance the ability of immune cells to destroy pathogens. When activated, complement components form the membrane attack complex, which disrupts the integrity of foreign cells, leading to their destruction. The complement system is essential for maintaining inflammatory responses, protecting against infections, and eliminating damaged cells. However, excessive complement activity can damage tissue and impair blood clotting, contributing to thrombosis.

Compared to fully recovered individuals, patients with post-COVID syndrome exhibit alterations in the levels of complement component C7 and the C5bC6 complex, necessary for membrane attack complex formation. The ratio of C5bC6/C7 is elevated during acute COVID-19 and post-COVID syndrome, confirming increased complement activity and immune system alterations during acute infection and long after recovery.

Increased complement activity contributes to thrombosis and tissue damage:

  • Patients with post-COVID syndrome demonstrate decreased levels of antithrombin III, which may contribute to thrombosis development.
  • Enhanced complement activity leads to erythrocyte destruction and thromboinflammatory reactions.
  • Post-COVID syndrome patients show elevated levels of blood clotting factor VIII and an increased ratio of low-density lipoproteins to high-density lipoproteins, which are risk factors for cardiovascular diseases.

The presence of autoantibodies, antibodies against herpes viruses, and tissue damage facilitates complement activation. Severe COVID-19 is associated with autoantibody formation and inflammation that persists after recovery. Post-COVID syndrome patients exhibit elevated antibodies to Epstein-Barr virus and cytomegalovirus, which may contribute to complement activation and the maintenance of post-COVID syndrome.

Antiviral drugs targeting coronaviruses and herpesviruses may alleviate thromboinflammatory reactions. Therapeutic agents directed at the complement system may benefit post-COVID syndrome treatment.

For further details, refer to the article “How the Complement System Contributes to Post-COVID Syndrome,” published in the Science journal.

Low Tryptophan Levels and Increased KYN/TRY Ratio

A study on post-COVID syndrome involving 60 patients revealed that inflammatory processes initiated during COVID-19 persist even after recovery, leading to physical and psycho-emotional symptoms. The critical biomarkers of the post-COVID syndrome were found to be elevated C-reactive protein (CRP), increased kynurenine to tryptophan ratio (KYN/TRY), and insulin resistance (IR). These markers are associated with chronic fatigue, anxiety, and somatic symptoms.

Blood tests were conducted to measure the levels of tryptophan, kynurenine, and CRP in the patients. Additionally, each patient’s medical history was reviewed to assess their blood oxygen levels (SpO2) and peak temperature during the acute phase of COVID-19. The results indicated that patients with more severe post-COVID syndrome had significantly lower tryptophan levels, higher CRP, and an elevated KYN/TRY ratio. One of the critical factors determining the severity of post-COVID syndrome was a low SpO2 during the acute phase of the illness.

A reduction in tryptophan, which is essential for serotonin synthesis, exacerbates physical and emotional symptoms. Early control of inflammatory processes may help prevent severe post-COVID syndrome.

Further details of the study can be found in the article “The Cause of Fatigue in Post-COVID Syndrome: Tryptophan Catabolites, Inflammation, and Insulin Resistance,” published in Frontiers in Molecular Neuroscience.

Shortness of Breath and Exercise Intolerance after COVID-19

Patients often experience fatigue, shortness of breath, and exercise intolerance after COVID-19. British Heart Foundation scientists investigated post-COVID syndrome in 159 patients over 14 months after hospitalization for COVID-19. The average age of patients was 55 years, and 46% had a history of cardiovascular disease. Coronavirus treatment groups:

  • 69% received oxygen;
  • 56% received steroids;
  • 26% received antiviral drug therapy;
  • 20% received non-invasive respiratory support;
  • 9% received invasive ventilation.

One in seven patients died or was re-hospitalized, and 68% of patients went to the hospital.

Scientists have found that patients with post-COVID syndrome develop chronic cardio-renal damage.

Myocarditis

Every eighth patient (13%) had myocarditis 28-60 days after COVID-19. The leading cause of myocarditis was coronavirus, less often coronary heart disease. Myocarditis, as a complication after COVID-19, has been associated with subsequent pulmonary fibrosis.

Myocardial scar tissue reduces the heart’s pumping function and is associated with a poor prognosis. After COVID-19, myocardial scars appeared in every fifth patient. Causes of scarring included myocarditis, microvascular thrombosis, and myocardial infarction.

Glycated hemoglobin (HbA1c) was inversely correlated with confirmed myocarditis. Glycated hemoglobin rises above average in diabetes mellitus and renal failure and decreases below normal in diseases associated with a shortened life span of red blood cells. Healthy people with low HbA1c tend to be hospitalized with more severe COVID-19 and, therefore, more myocardial damage. However, patients with cardiovascular risk factors and higher HbA1c levels are hospitalized earlier, with relatively milder COVID-19. The inverse correlation of HbA1c levels with myocarditis can be explained by systemic inflammation, which leads to anemia and reduced erythrocyte survival.

Acute kidney injury

Acute kidney injury (AKI) is associated with mortality from COVID-19. Confirmed myocarditis was associated with AKI on admission and signs of inflammation in the renal medulla 28-60 days after discharge. This association can be explained by systemic inflammation, activation of the blood coagulation system, microvascular dysfunction, and chronic COVID-19 infection.

In clinical practice, the biomarker NT-proBNP, a brain natriuretic propeptide, the level of which increases with heart failure, can be used to assess risk in COVID-19 and during the rehabilitation period.

Diagnosis of myocarditis

The post-COVID syndrome develops more often in women. The likelihood of myocarditis with coronavirus is also higher in women. Myocarditis was associated with impaired contractility of the left ventricle.

An increase in troponin can diagnose myocarditis. However, troponin levels can increase not only due to myocardial damage but also due to hypoxia, hypotension, ischemia, and renal failure. Therefore, the clinical assessment of patients with COVID-19 and cardiopulmonary symptoms should include a detailed history, examination with heart rate measurements, heart rate, blood pressure, auscultation, and a 12-lead electrocardiogram. In the presence of cardiovascular disease or suspected heart damage, troponin levels should be measured. If troponin is elevated, echocardiography is necessary. Pericardial chest pain, saddle ST elevation on the ECG, and ventricular arrhythmias support the possibility of myocarditis. In this case, an MRI of the heart should be performed.

Post-COVID Chronic Fatigue

Constant fatigue is one of the symptoms of the post-COVID syndrome. A recent study by American scientists showed that half of the patients with post-COVID syndrome suffer from chronic fatigue.

How to Recognize Chronic Fatigue Syndrome – Fukuda Criteria, 1994:

  1. Unexplained, persistent or recurring fatigue, which was not there before and is not the result of constant stress, does not disappear after rest and leads to a significant decrease in the previous level of professional, educational, social and personal activity.
  2. Simultaneous occurrence of four or more symptoms from the list below, symptoms persist or recur for 6 or more consecutive months and do not precede fatigue:
    • violation of short-term memory or concentration of attention, significantly reducing the previous level of professional, educational, social and personal activity;
    • sore throat;
    • soreness of the cervical or axillary lymph nodes;
    • muscle or multi-joint pain without swelling or redness of the joints;
    • headaches of a new type, change in the severity of headaches;
    • the condition does not improve after sleep;
    • feeling unwell after exercising for more than 24 hours.

Fatigue is associated with disruption of the brain’s glymphatic system. The glymphatic system eliminates waste from the brain. When its functioning is disrupted, the cerebrospinal fluid stagnates, and toxins accumulate in the central nervous system (CNS).

Coronavirus can affect skeletal muscles, causing inflammation of muscle fibers, neuromuscular junctions and mitochondrial dysfunction. All this can also contribute to weakness, fatigue and exercise intolerance.

Vagus Nerve Stimulation to Treat Fatigue after COVID-19

Scientists at the Icahn School of Medicine at Mount Sinai (USA) investigated whether vagus nerve stimulation can help patients with post-COVID chronic fatigue.

The study included 14 coronavirus survivors with chronic fatigue that met the Fukuda criteria.

The vagus nerve was stimulated with a device attached to the ear’s tragus and generated electrical impulses. The impulses act on the ear branch of the vagus nerve, which is located close to the skin in the tragus region. Patients stimulated the vagus nerve for 35 minutes daily for 6 weeks.

Research Results

In 57% of patients, the condition improved: physical functioning increased on the SF-36 scale, and the severity of the most disturbing symptom and the level of fatigue decreased. There were no side effects.

The only symptom of vagus nerve stimulation did not affect impaired short-term memory or concentration.

There was no control group in the study, so the placebo effect could explain the positive result. However, a review of trials for treating chronic fatigue syndrome showed that the highest positive rate for placebo was 24%, while the present study showed an improvement rate of 57%.

Dysfunction of the Interferon System Does Not Play a Significant Role in Post-COVID-19 Fatigue

Some COVID-19 patients are found to have autoantibodies that block the action of interferons. These autoantibodies are associated with severe cases of COVID-19. A group of scientists from Germany and Switzerland investigated whether autoantibodies against interferons cause chronic fatigue in post-COVID syndrome.

The study included 128 patients experiencing fatigue lasting more than 12 weeks after COVID-19. Control groups included patients without chronic fatigue after coronavirus and patients with severe COVID-19.

In patients with chronic fatigue after COVID-19:

  • No autoantibodies to IFN-α2 were found.
  • Autoantibodies to IFN-β were found in only 1.6% of patients and exhibited weak neutralizing activity.
  • Autoantibodies to IFN-ω were found in 4.7% of patients, but only one showed neutralizing activity.

Autoantibodies to type I interferons in patients with post-COVID syndrome are found at the same frequency as in the general population. Among people under 70, autoantibodies to type I interferons are present in 0.2-1.1% of cases. The level of autoantibodies to type I interferons is not associated with fatigue in post-COVID syndrome and dysfunction of the interferon system does not play a significant role in the development of fatigue after COVID-19.

Details of the study are presented in the article “Autoantibodies to Interferons Are Not Associated with Chronic Fatigue after COVID-19.” The study was published in the journal Open Forum Infectious Diseases.

Impairment of Cognitive and Mental Functions in Post-COVID Syndrome

  • The coronavirus penetrates the central nervous system, causing the permeability of the blood-brain barrier (BBB) to increase. Through the permeable BBB, inflammatory cytokines enter the CNS and cause neuroinflammation.
  • Patients with post-COVID syndrome have altered brain microstructure. The thickness of the cortex is reduced, the microstructure of the white matter is changed, and regional blood flow is reduced, especially in the frontal lobe and limbic system.
  • Impaired taste and smell in patients with post-COVID syndrome may result from coronavirus penetration into the olfactory cells. Coronavirus causes inflammation and, as a result, a change in the taste threshold.

Rehabilitation of Patients with Post-COVID Syndrome

At the beginning of rehabilitation, red flags should be excluded: decreased blood oxygen saturation during physical activity and abnormal heart rhythm. If red flags are identified, the underlying pathology should be treated first.

Once red flags have been ruled out, screening for orthostatic intolerance and post-exercise symptom exacerbation should be performed. Worsening of symptoms may occur immediately or 12-72 hours after exercise and last from several hours to several weeks.

In patients with exacerbation of symptoms following exercise, the onset, duration, and intensity of the exacerbation should be monitored and potential precipitating factors investigated. Training in self-help methods is offered to reduce exacerbation: breathing techniques, stress management, and life optimization. A sudden increase in rehabilitation intensity should be avoided.

Patients with orthostatic intolerance should drink enough fluids and salt and avoid triggers such as prolonged standing, heat and large meals. Compression stockings, an abdominal band, and pharmacological interventions may be used. Regular aerobic exercise in a non-vertical position is preferable to avoid orthostatic intolerance: swimming, recumbent stationary bicycle, and weight training.

Psychotherapy and pharmacological therapy are recommended for patients with mental disorders and sleep disorders. Mindfulness-based stress reduction (MBSR) may help reduce anxiety, depression, and sleep problems. Exercise also relieves mental disorders. Cognitive stimulation, environmental modification, and cognitive restorative exercises can be used to treat cognitive impairment.

Read more about rehabilitation in the article “Post-COVID syndrome: rehabilitation.” The review was published in the Journal of the Formosan Medical Association.

Treating Post-COVID Syndrome

Dexamethasone, an anti-inflammatory glucocorticoid, may reduce the risk of myocarditis.

Antithrombotic therapy can prevent post-COVID syndrome in hospitalized patients with COVID-19 since the blood coagulation system is activated in post-COVID syndrome.

Empagliflozin. Immunomodulatory drugs, such as the Janus kinase inhibitor baricitinib and the sodium-glucose cotransporter type 2 inhibitor empagliflozin, have beneficial effects in patients with type 2 diabetes at high cardiovascular risk.

Vagus nerve stimulation improves the condition of patients with post-COVID chronic fatigue and may also reduce inflammation by suppressing the production of inflammatory cytokines.

Vaccination. Data from the UK Office for National Statistics show that people who received two doses of the coronavirus vaccine were 41% less likely to develop the post-COVID syndrome.

Blocking IFN-γ: A New Approach to Treating Post-COVID Syndrome

The coronavirus primarily affects the lungs, which is why many individuals who have recovered from COVID-19 continue to experience respiratory issues such as shortness of breath and coughing. These symptoms are indicative of respiratory post-COVID syndrome. Impaired gas exchange can lead to exercise intolerance and chronic fatigue due to persistent hypoxia. These symptoms can last for over two years, particularly following severe cases of COVID-19.

Researchers at the University of Virginia in the United States have discovered that interferon-gamma (IFN-γ) plays a key role in the development of respiratory post-COVID syndrome. IFN-γ attracts and activates monocytes, which transform into inflammatory macrophages that damage lung tissue and contribute to fibrosis development.

Blocking IFN-γ in mice reduced lung inflammation and fibrosis, improving the condition of the mice after COVID-19. As a result, Janus kinase inhibitors, such as baricitinib, may be promising for the treatment of patients with respiratory post-COVID syndrome.

Details of the study can be found in the article titled “Interferon-γ Contributes to Respiratory Complications After COVID-19,” published in the journal Science Translational Medicine.

Physical Therapy for Post-COVID Syndrome

Exercise can help overcome fatigue, exercise intolerance, shortness of breath, mental health and sleep problems, and muscle and joint pain.

For patients with post-COVID syndrome, exercise therapy is recommended for 6-8 weeks. Exercise therapy for post-COVID syndrome includes:

  • aerobic exercises;
  • weight training;
  • training of respiratory muscles.

The effectiveness of exercise therapy was confirmed by a randomized controlled trial involving 39 patients with post-COVID syndrome after a mild form of COVID-19. For 8 weeks, the intervention group performed supervised low-to-moderate intensity aerobic and resistance exercises. The control group maintained general physical activity following WHO recommendations, without supervised exercise. In the intervention group, mean maximum oxygen consumption (VO2) increased by 5.7%. In the control group, BMD did not change. 42.1% of participants in the intervention group reported being symptom-free at 8 weeks. In the control group – only 16.7%. Exercise resulted in significant improvements in quality of life, decreased fatigue, decreased depression, improved functional status, and improvements in cardiovascular health and muscle strength compared with the control group.

Post-COVID Syndrome in Children

Rehabilitation of children with post-COVID syndrome includes:

  • aerobic exercises;
  • weight training;
  • relaxation exercises;
  • exercises for the lungs;
  • treatment of postural orthostatic tachycardia syndrome;
  • cognitive training;
  • psychological and social rehabilitation for returning to school.

Conclusions

The post-coagulant syndrome includes chronic inflammation of the cardiovascular system, lung damage, activation of the blood coagulation system, and impairment of physical and mental functions. Every 7th patient with post-COVID syndrome died or was re-hospitalized, and every 2 out of 3 patients went to the hospital. Prevention and treatment of post-COVID syndrome and vaccination can reduce mortality and improve patients’ quality of life who have had COVID-19.

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