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Do You Know About the Multi-organ Effects of Post-Acute Coronavirus (COVID-19) Syndrome?

Multi-organ Effects of Post-Acute Coronavirus (COVID-19) Syndrome

COVID-19 is primarily a respiratory viral infection caused by the SARS-CoV-2 virus. COVID-19 is now considered a systemic illness based on the broad-spectrum clinical manifestations associated with the involvement of multiple organs in patients infected with SARS-CoV-2. COVID-19’s immediate complications are well-defined and are frequently associated with increased mortality. However, delayed or long-term COVID-19 complications are becoming more common and are associated with increased morbidity.

Because of severe damage to multiple organs, SARS-CoV-2 has caused terrible global morbidity and mortality rates. Even though many people survive the acute phase of COVID-19, there is mounting evidence that the long-term effects of SARS-CoV-2 infection can have an impact on a person’s quality of life and ability to return to work. Dyspnea, fatigue, loss of taste and smell, cognitive impairment, chest pain, and arthralgia are all common long-term symptoms.

Coronaviruses are RNA viruses with a positive strand that primarily affect the respiratory tract. Because the virus can access human type II alveolar cells via the angiotensin-converting enzyme 2, the lungs are particularly vulnerable (ACE2). Because it cannot reproduce on its own, the SARS-CoV relies on specific host cell factors throughout its infection cycle. The virus replicates within cells by hijacking the body’s own cellular machinery and binding to the ACE2 receptor.

To enter the host cell, SARS-CoV-2 has surface glycoproteins called spikes that connect to the ACE2 receptor. The viral element that attaches to the host receptor via the ACE2 receptors is known as the S-protein spike, and there are two subunit S-proteins known as S1 and S2. The receptor-binding domain of the S1 protein determines the virus-host range and cellular tropism by binding to the host receptor ACE2.

Once on the ACE2 cell surface, the virus induces leukocytic infiltration, increases alveolar wall and blood vessel permeability, and decreases lung surfactants. This causes respiratory symptoms and inflammation, which can lead to a cytokine storm and, ultimately, a systemic inflammatory response syndrome. By forming a six-helical bundle, the S2-protein mediates virus-cell fusion via the H1 and HR2 receptors. The S1 domain is responsible for the induction of immunoglobin G and immunoglobulin A antibody activity. The M-protein of SARs-CoV-2 regulates nutrient transmembrane transport and viral envelope formation. N- and E-proteins, on the other hand, limit the host’s immune response.

Persistent symptoms such as fatigue, diffuse myalgia, and joint and musculoskeletal pain have been reported in surveys of people suffering from the post-COVID-19 syndrome. All of these symptoms are linked to mitochondrial dysfunction, oxidative stress, and low antioxidant levels. The mitochondria may play a role in the pathophysiology and treatment of fatigue associated with the post-COVID-19 syndrome. To compensate for dysfunctional oxidative phosphorylation, mitochondrial bioenergetic dysfunction may result in anaerobic glycolysis. Glycolysis causes cellular damage, and it can inhibit lactate levels and other metabolic pathways.

One possible explanation for muscle aches and fatigue is that the virus infects neurons selectively in order to evade the host’s immune system. SARS CoV-2 can infiltrate the host immune system by entering a dormant state with low replication while infecting neurons. Inflammasome activation, which is part of the innate immune system receptors, has been linked to a cytokine storm and hypercoagulopathy in the infected host. As a result, the person with the post-COVID-19 syndrome may have lifelong infections that can be reactivated whenever the host’s immune system is weakened.


The respiratory, cardiovascular, and hematopoietic systems are commonly affected in post-acute COVID-19 syndrome. Furthermore, the neuropsychiatric, renal, and endocrine systems are all involved to varying degrees. The following sections describe significant organ-specific histopathology findings.













Coexisting conditions such as diabetes, chronic kidney disease, and hypertension should be treated as well. Patients should be taught how to self-monitor at home using FDA-approved devices such as a pulse oximeter, blood pressure monitors, and blood glucose monitors. Patients should be encouraged to eat a healthy, balanced diet, practice good sleep hygiene, limit alcohol consumption, and quit smoking. If tolerated, a structured exercise program with aerobic and resistance components should be recommended, assuming that there are no other contraindications. Simple analgesia with acetaminophen should be considered as needed.

Pulmonology: Patients who have persistent symptoms may benefit from enrolling in a pulmonary rehabilitation program, which is essential for faster clinical recovery, and vaccination against influenza and Streptococcus pneumonia.

Cardiology: To rule out arrhythmias, heart failure, and ischemic heart disease, cardiac function tests such as EKG and echocardiography must be considered. If clinically indicated, an MRI of the heart can be considered to evaluate for myocardial fibrosis or scarring.

Haematology: Current CHEST guidelines recommend that COVID-19 patients who develop proximal deep vein thrombosis or pulmonary embolism receive anticoagulation therapy for at least 3 months.

Neuropsychiatric: If there are concerns about seizures or paresthesia, EEG and EMG should be considered. Patients should be screened for common psychological issues like anxiety, depression, and insomnia, and HbA1c, TSH, thiamine, folate, Vitamin B12, and Vitamin B12 levels should be checked to rule out other contributing metabolic conditions.

Post-acute COVID-19 syndrome is a growing complication of COVID-19, and secondary complications associated with this syndrome are currently unknown. More clinical data is needed to fully comprehend the long-term consequences of this syndrome.

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