1.
Long COVID: An overview.
Raveendran, AV, Jayadevan, R, Sashidharan, S
Diabetes & metabolic syndrome. 2021;15(3):869-875
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SARS-CoV-2 infection (COVID-19) is a major pandemic resulting in considerable mortality and morbidity worldwide. For some people who recover from COVID-19, symptoms persist or new ones develop for weeks or months after infection despite testing PCR negative. This is termed long-COVID or post-COVID syndrome and divided into two stages: post-acute-COVID with symptoms extending beyond three weeks, and chronic-COVID with symptoms extending beyond 12 weeks. Factors that increase the risk for long-COVID include being female, age, having more than five symptoms in the acute stage of infection and pre-existing health conditions. A mild disease course is not exclusive to long-COVID. Typically affected by long-COVID are the pulmonary or cardiovascular system, with neuropsychiatric presentations also being reported. Common symptoms are one or more of the following such as fatigue, breathlessness, cough, chest pain, heart racing, headache, joint pain, muscle pain and weakness, insomnia, pins and needles, diarrhoea, rash, hair loss, impaired balance, neurocognitive issues. Due to the novelty of the virus, the underline pathophysiology of long-COVID still requires further investigation. Contributing factors mentioned include: compromised body functions after illness and inactivity, organ damage, persistent inflammation, altered immune response and auto-antibody generation and viral persistence. The impact of medication, treatments, hospitalisation or associated post-traumatic stress is also urged to be accounted for. Diagnosis of long-COVID is made by thorough history taking, clinical examination and the exclusion of other conditions. For the management of long-COVID, the authors in this review suggest the sub-categorisation depending on the body system most affected to optimize treatment options. Furthermore, it is encouraged that medical treatment should also consider the monitoring for worsening of any pre-existing health conditions post-infection. This review yields a informative summary of the definition, symptom presentations, risk factors, diagnosis and medical treatment options relating to long-COVID.
Abstract
BACKGROUND AND AIMS Long COVID is the collective term to denote persistence of symptoms in those who have recovered from SARS-CoV-2 infection. METHODS WE searched the pubmed and scopus databases for original articles and reviews. Based on the search result, in this review article we are analyzing various aspects of Long COVID. RESULTS Fatigue, cough, chest tightness, breathlessness, palpitations, myalgia and difficulty to focus are symptoms reported in long COVID. It could be related to organ damage, post viral syndrome, post-critical care syndrome and others. Clinical evaluation should focus on identifying the pathophysiology, followed by appropriate remedial measures. In people with symptoms suggestive of long COVID but without known history of previous SARS-CoV-2 infection, serology may help confirm the diagnosis. CONCLUSIONS This review will helps the clinicians to manage various aspects of Long COVID.
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Persistent fatigue following SARS-CoV-2 infection is common and independent of severity of initial infection.
Townsend, L, Dyer, AH, Jones, K, Dunne, J, Mooney, A, Gaffney, F, O'Connor, L, Leavy, D, O'Brien, K, Dowds, J, et al
PloS one. 2020;15(11):e0240784
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Tiredness is a common symptom of Covid-19; however, it is unknown if this fatigue persists once recovered. This observational study of 128 recovered Covid-19 patients aimed to determine if fatigue persisted after recovery and whether severity of disease could predict fatigue. The results showed that post Covid-19 fatigue was reported in more than half of the participants and was particularly pronounced in females and in those with depression. Severity of disease did not predict fatigue. It was concluded that fatigue appears to outlast infection and fatigue was independent of disease severity. This study could be used by health care practitioners to understand that fatigue is common even after recovery from Covid-19 infection and women and sufferers of depression are the most susceptible.
Abstract
Fatigue is a common symptom in those presenting with symptomatic COVID-19 infection. However, it is unknown if COVID-19 results in persistent fatigue in those recovered from acute infection. We examined the prevalence of fatigue in individuals recovered from the acute phase of COVID-19 illness using the Chalder Fatigue Score (CFQ-11). We further examined potential predictors of fatigue following COVID-19 infection, evaluating indicators of COVID-19 severity, markers of peripheral immune activation and circulating pro-inflammatory cytokines. Of 128 participants (49.5 ± 15 years; 54% female), more than half reported persistent fatigue (67/128; 52.3%) at median of 10 weeks after initial COVID-19 symptoms. There was no association between COVID-19 severity (need for inpatient admission, supplemental oxygen or critical care) and fatigue following COVID-19. Additionally, there was no association between routine laboratory markers of inflammation and cell turnover (leukocyte, neutrophil or lymphocyte counts, neutrophil-to-lymphocyte ratio, lactate dehydrogenase, C-reactive protein) or pro-inflammatory molecules (IL-6 or sCD25) and fatigue post COVID-19. Female gender and those with a pre-existing diagnosis of depression/anxiety were over-represented in those with fatigue. Our findings demonstrate a significant burden of post-viral fatigue in individuals with previous SARS-CoV-2 infection after the acute phase of COVID-19 illness. This study highlights the importance of assessing those recovering from COVID-19 for symptoms of severe fatigue, irrespective of severity of initial illness, and may identify a group worthy of further study and early intervention.
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Viruses belonging to Anelloviridae or Circoviridae as a possible cause of chronic fatigue.
Grinde, B
Journal of translational medicine. 2020;18(1):485
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Chronic fatigue syndrome (CFS) is often triggered by a virus. This review argues that viruses already present in the body may be the cause of this condition and identifies two groups of viruses the anello and circoviruses as potential causes. The paper explains that both viruses are already present in many individuals, and only become a problem when the immune system is supressed by a secondary infection. When this happens the anello and circoviruses can penetrate the brain resulting in CFS. Therapies that inhibit these viruses are required and recently certain antimalarials have reported to be potential candidates. Further research is required. This study could be used by healthcare professionals to extend research into the role of viruses that are already present within the body on CFS.
Abstract
Chronic fatigue often starts with an acute viral infection-as witnessed in the case of SARS-CoV-2-but indirect consequences of these infections are presumably the actual cause of the condition. As recently reviewed in this journal, the culprit could be a virus already present in the patient. The review covers several types of viruses, but concludes that the question is still open. The focus is on well known, pathogenic viruses for which there are ample diagnostic tools. I argue that there is one lesser-known group of viruses, the related anello- and circoviruses, which ought to be investigated. More or less everyone harbours at least one strain of these viruses in the blood, while not in the spinal fluid. They normally replicate at a low level, but their activity increases in an immune suppressed host; and there are cases where they do reach the brain. The initial infection could facilitate their access to the brain.
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Will COVID-19 Lead to Myalgic Encephalomyelitis/Chronic Fatigue Syndrome?
Komaroff, AL, Bateman, L
Frontiers in medicine. 2020;7:606824
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In people who have contracted COVID-19, many do not return to full health. Some may develop permanent dysfunction of damaged organs such as the brain, heart and kidney. Others report ongoing lingering symptoms despite tests no longer detecting the virus. This condition is being called ‘long covid.’ Patients post-COVID-19 can develop a post-viral syndrome that is very similar to Myalgic Encephalomyelitis/Chronic Fatigue syndrome, (ME/CFS). This short review looks at how common a post covid illness is and what implications this has for the U.S. and globally. The review concludes that the U.S. and the world will see a substantial growth in the number of people with ME/CFS. We can’t predict at this stage how long lasting that will be.
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Clinical symptoms and markers of disease mechanisms in adolescent chronic fatigue following Epstein-Barr virus infection: An exploratory cross-sectional study.
Kristiansen, MS, Stabursvik, J, O'Leary, EC, Pedersen, M, Asprusten, TT, Leegaard, T, Osnes, LT, Tjade, T, Skovlund, E, Godang, K, et al
Brain, behavior, and immunity. 2019;80:551-563
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Epstein-Barr virus (EBV) can trigger chronic fatigue (CF) and chronic fatigue syndrome (CFS) in individuals who are predisposed. However, how fatigue develops and how infections may trigger this is not fully understood. This exploratory cross-sectional study of 200 fatigued and non-fatigued adolescents 6 months after EBV aimed to understand symptoms and potential markers for disease. The results showed that all symptoms (not just fatigue) were more pronounced in those individuals suffering from fatigue, despite no increases in viral load. Those with fatigue only had slight changes in immune, nerve and hormonal markers and none correlated with severity of symptoms. It was concluded that there is a discrepancy between symptoms and viral load and alterations to several markers were only marginal. This study could be used by healthcare professionals to understand the possible limitations of using several biomarkers as a diagnostic tool for CF and CFS.
Abstract
INTRODUCTION Acute Epstein-Barr virus (EBV) infection is a trigger of chronic fatigue (CF) and Chronic Fatigue Syndrome (CFS). The aim of this cross-sectional study was to explore clinical symptoms as well as markers of disease mechanisms in fatigued and non-fatigued adolescents 6 months after EBV-infection, and in healthy controls. MATERIALS AND METHODS A total of 200 adolescents (12-20 years old) with acute EBV infection were assessed 6 months after the initial infectious event and divided into fatigued (EBV CF+) and non-fatigued (EBV CF-) cases based on questionnaire score. The EBV CF+ cases were further sub-divided according to case definitions of CFS. In addition, a group of 70 healthy controls with similar distribution of sex and age was included. Symptoms were mapped with a questionnaire. Laboratory assays included EBV PCR and serology; detailed blood leukocyte phenotyping and serum high-sensitive C-reactive protein; and plasma and urine cortisol and catecholamines. Assessment of autonomic activity was performed with continuous, non-invasive monitoring of cardiovascular variables during supine rest, controlled breathing and upright standing. Differences between EBV CF+ and EBV CF- were assessed by simple and multiple linear regression adjusting for sex as well as symptoms of depression and anxiety. A p-value ≤ 0.05 was considered statistically significant. This study is part of the CEBA-project (Chronic fatigue following acute Epstein-Barr virus infection in adolescents). RESULTS The EBV CF+ group had significantly higher scores for all clinical symptoms. All markers of infection and most immune, neuroendocrine and autonomic markers were similar across the EBV CF+ and EBV CF- group. However, the EBV CF+ group had slightly higher serum C-reactive protein (0.48 vs 0.43 mg/L, p = 0.031, high-sensitive assay), total T cell (CD3+) count (median 1573 vs 1481 × 106 cells/L, p = 0.012), plasma norepinephrine (1420 vs 1113 pmol/L, p = 0.01) and plasma epinephrine (363 vs 237 nmol/L, p = 0.032); lower low-frequency:high frequency (LF/HF) ratio of heart rate variability at supine rest (0.63 vs 0.76, p = 0.008); and an attenuated decline in LF/HF ratio during controlled breathing (-0.11 vs -0.25, p = 0.002). Subgrouping according to different CFS diagnostic criteria did not significantly alter the results. Within the EBV CF+ group, there were no strong correlations between clinical symptoms and markers of disease mechanisms. In a multiple regression analysis, serum CRP levels were independently associated with serum cortisol (B = 4.5 × 10-4, p < 0.001), urine norepinephrine (B = 9.6 × 10-2, p = 0.044) and high-frequency power of heart rate variability (B = -3.7 × 10-2, p = 0.024). CONCLUSIONS In adolescents, CF and CFS 6 months after acute EBV infection are associated with high symptom burden, but no signs of increased viral load and only subtle alterations of immune, autonomic, and neuroendocrine markers of which no one is strongly correlated with symptom scores. A slight sympathetic over parasympathetic predominance is evident in CF and might explain slightly increased CRP levels.