COVID-19 is a SARS-CoV-2 viral infection mainly affecting the respiratory system, with initial signs of fever, cough, and body ache. As of Sep 9 (th) 2020, there have been more than 27.6 million confirmed cases worldwide, and over 898,000 died. Fatigue is a widely recorded symptom of COVID-19 (1), although observational evidence suggests that certain individuals persist in encountering intense amounts of chronic fatigue as they recuperate from this infection.
The recovery process is not yet fully understood. Some patients develop Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) after the acute SARS episode. The symptoms of CFS/ME are persistent fatigue, myalgia, depressive symptoms and nonrestorative sleep. Fatigue was one of the most often encountered consequences of the COVID-19 survivors. Approximately 53% of individuals displayed fatigue, with no marked difference in ethnicity or body mass index (BMI). There was no difference in the age within the ICU group (2, 3).
Post-infectious fatigue has likewise been witnessed after other epidemics, such as SARS-CoV1virus, the influenza A (H1N1) and Ebolavirus infection. Given the sufficient data from earlier epidemics, many COVID-19 survivors may encounter post-viral fatigue. However, the factors which influence such development are uncertain. The recent research has demonstrated the involvement of the cytokine response. Mehta et al. (4) observed a 'cytokine storm' in patients with COVID-19. Elevated levels of IL-2, IL-7, granulocyte-colony stimulating factor, interferon-[gamma] inducible protein10, monocyte chemoattractant protein 1, [alpha] macrophage inflammatory protein and [alpha] tumor necrosis factor were found in these patients (4). These results suggest a...
This is a preview. Get the full text through your school or public library.