Journal articles: 'Post Viral Fatigue Syndrome'

1

Greenberg, Donna B. "Post-viral Fatigue Syndrome." Psychosomatics 33, no. 1 (February 1992): 114–16. http://dx.doi.org/10.1016/s0033-3182(92)72031-3.

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Dunn, M. G. "Post-Viral Fatigue Syndrome." Archives of Neurology 52, no. 10 (October 1, 1995): 943–44. http://dx.doi.org/10.1001/archneur.1995.00540340019008.

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Loudon, Michael F. "Post-viral Fatigue Syndrome." JAMA: The Journal of the American Medical Association 267, no. 11 (March 18, 1992): 1539. http://dx.doi.org/10.1001/jama.1992.03480110131044.

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Powell, R. J. "Post Viral Fatigue Syndrome." Postgraduate Medical Journal 69, no. 811 (May 1, 1993): 414. http://dx.doi.org/10.1136/pgmj.69.811.414-a.

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Beal, Jane. "Post viral fatigue syndrome." Behaviour Research and Therapy 31, no. 2 (February 1993): 225. http://dx.doi.org/10.1016/0005-7967(93)90085-9.

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Lefkowitz, David S. "Post-viral fatigue syndrome." Journal of the Neurological Sciences 108, no. 1 (March 1992): 118. http://dx.doi.org/10.1016/0022-510x(92)90197-s.

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Shepherd, Simon. "Post-viral fatigue syndrome." Journal of Psychosomatic Research 36, no. 7 (October 1992): 695–96. http://dx.doi.org/10.1016/0022-3999(92)90061-6.

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Fegan, K. E. "M.E.--Post viral fatigue syndrome." British Journal of Sports Medicine 22, no. 3 (September 1, 1988): 119–20. http://dx.doi.org/10.1136/bjsm.22.3.119.

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Foster, J. "BOOK REVIEWS: Post-Viral Fatigue Syndrome." Journal of Neurology, Neurosurgery & Psychiatry 55, no. 1 (January 1, 1992): 85–86. http://dx.doi.org/10.1136/jnnp.55.1.85-b.

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Ho-Yen, D. O. "The Epidemiology of Post Viral Fatigue Syndrome." Scottish Medical Journal 33, no. 6 (December 1988): 368–69. http://dx.doi.org/10.1177/003693308803300607.

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The epidemiology of the post viral fatigue syndrome was studied for the years 1985–86. With a strict definition of the syndrome, it was found that there were many misconceptions about this illness. The sex incidence was nearly equal with a similar pattern of twin peaks at 25–29 years and 40–45 years. At diagnosis, 56% were ill for three to six months and only 9% for more than two years. It is estimated that this syndrome is more common than infectious mononucleosis.

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Shearman, David. "Global view of post‐viral fatigue syndrome." Medical Journal of Australia 156, no. 5 (March 1992): 361. http://dx.doi.org/10.5694/j.1326-5377.1992.tb139804.x.

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Lapp, Charles W., and Joseph F. John. "Managing COVID-19 post viral Fatigue Syndrome." Fatigue: Biomedicine, Health & Behavior 9, no. 1 (January 2, 2021): 1–8. http://dx.doi.org/10.1080/21641846.2021.1890347.

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Smilack, Jerry D. "Reviews and Notes: Virology: Post-viral Fatigue Syndrome; and Chronic Fatigue Syndrome." Annals of Internal Medicine 120, no. 5 (March 1, 1994): 445. http://dx.doi.org/10.7326/0003-4819-120-5-199403010-00038.

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Jamal, G. A., and S. Hansen. "Electrophysiological studies in the post-viral fatigue syndrome." Journal of Neurology, Neurosurgery & Psychiatry 48, no. 7 (July 1, 1985): 691–94. http://dx.doi.org/10.1136/jnnp.48.7.691.

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Lynch, Sean. "Chronic fatigue syndrome." Advances in Psychiatric Treatment 1, no. 2 (November 1994): 33–40. http://dx.doi.org/10.1192/apt.1.2.33.

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“Chronic fatigue syndrome” (Sharpeet al, 1991) is an operational definition for conditions of disabling physical fatigue, of over six months duration, unexplained by primary physical or psychiatric causes. It encompasses nomenclature such as “myalgic encephalomyelitis” (Acheson, 1959), “post-viral fatigue syndrome” (Behanet al, 1985) and “chronic mononucleosis syndrome” (Straus, 1988).

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Ostojic, Sergej M. "Diagnostic and Pharmacological Potency of Creatine in Post-Viral Fatigue Syndrome." Nutrients 13, no. 2 (February 4, 2021): 503. http://dx.doi.org/10.3390/nu13020503.

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Post-viral fatigue syndrome (PVFS) is a widespread chronic neurological disease with no definite etiological factor(s), no actual diagnostic test, and no approved pharmacological treatment, therapy, or cure. Among other features, PVFS could be accompanied by various irregularities in creatine metabolism, perturbing either tissue levels of creatine in the brain, the rates of phosphocreatine resynthesis in the skeletal muscle, or the concentrations of the enzyme creatine kinase in the blood. Furthermore, supplemental creatine and related guanidino compounds appear to impact both patient- and clinician-reported outcomes in syndromes and maladies with chronic fatigue. This paper critically overviews the most common disturbances in creatine metabolism in various PVFS populations, summarizes human trials on dietary creatine and creatine analogs in the syndrome, and discusses new frontiers and open questions for using creatine in a post-COVID-19 world.

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Vorobyova, Yu D., and G. M. Diukova. "Asthenic syndrome in context of COVID-19 pandemic." Medical alphabet, no. 33 (January 14, 2021): 26–34. http://dx.doi.org/10.33667/2078-5631-2020-33-26-34.

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The article is devoted to the current problems of fatigue during the new coronavirus infection pandemic. The pathogenetic mechanisms of fatigue in the acute period of infection are considered, as well as potential mechanisms and factors influencing post-viral fatigue development after COVID-19 infection. A biopsychosocial approach to the pathogenesis and treatment of post-viral fatigue is proposed. In conclusion, the factors contributing to quarantine fatigue development and methods of its therapy are considered.

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Ho-Yen, Darrel O., Robert W. Billington, and Jack Urquhart. "Natural Killer Cells and the Post Viral Fatigue Syndrome." Scandinavian Journal of Infectious Diseases 23, no. 6 (January 1991): 711–16. http://dx.doi.org/10.3109/00365549109024298.

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Hartnell, Linda. "POST-VIRAL FATIGUE SYNDROME: A CANKER IN MY BRAIN." Lancet 329, no. 8538 (April 1987): 910. http://dx.doi.org/10.1016/s0140-6736(87)92873-x.

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Horrobin, D. F. "Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids." Medical Hypotheses 32, no. 3 (July 1990): 211–17. http://dx.doi.org/10.1016/0306-9877(90)90125-x.

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Hotchin, N. A., R. Read, D. G. Smith, and D. H. Crawford. "Active Epstein-Barr virus infection in post-viral fatigue syndrome." Journal of Infection 18, no. 2 (March 1989): 143–50. http://dx.doi.org/10.1016/s0163-4453(89)91150-x.

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Holloway, Elizabeth. "ME and You: A survivor's guide to post-viral fatigue syndrome." Physiotherapy 75, no. 3 (March 1989): 198. http://dx.doi.org/10.1016/s0031-9406(10)62818-0.

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Mears, Tim. "Acupuncture in the Treatment of Post Viral Fatigue Syndrome – a Case Report." Acupuncture in Medicine 23, no. 3 (September 2005): 141–45. http://dx.doi.org/10.1136/aim.23.3.141.

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This case report concerns the treatment of post viral fatigue (chronic fatigue syndrome) with electroacupuncture. This condition is particularly difficult to treat whether using conventional or complementary therapy. Whilst the treatment did not cure the patient, it appears to have facilitated her return to work and markedly improved her symptoms. There are few publications on acupuncture treatment of this condition and the approach used here has not been reported previously.

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Wilson, Clare. "Concern coronavirus may trigger post-viral fatigue syndromes." New Scientist 246, no. 3278 (April 2020): 10–11. http://dx.doi.org/10.1016/s0262-4079(20)30746-6.

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Cope, H., A. Mann, A. Pelosi, and A. David. "Psychosocial risk factors for chronic fatigue and chronic fatigue syndrome following presumed viral illness: a case–control study." Psychological Medicine 26, no. 6 (November 1996): 1197–209. http://dx.doi.org/10.1017/s0033291700035923.

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SynopsisThis study investigated psychosocial morbidity, coping styles and health locus of control in 64 cases with and without chronic fatigue identified from a cohort of primary care patients recruited 6 months previously with a presumed, clinically diagnosed viral illness. A significant association between chronic fatigue and psychosocial morbidity, somatic symptoms and escape-avoidance coping styles was shown. Chronic fatigue cases were significantly more likely to have a past psychiatric history and a current psychiatric diagnosis based on a standardized clinical interview. Twenty-three of the cases fulfilled criteria for chronic fatigue syndrome (CFS). Such cases were significantly more fatigued than those not fulfilling criteria, but had little excess psychiatric disorder. A principal components analysis provided some evidence for chronic fatigue being separable from general psychosocial morbidity but not from the tendency to have other somatic complaints. Past psychiatric history and psychological distress at the time of the viral illness were risk factors for psychiatric ‘caseness’ 6 months later, while presence of fatigue, psychologising attributional style and sick certification were significant risk factors for CFS. These findings extend a previous questionnaire study of predictors of chronic ‘post-viral’ fatigue.

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Bruno, Richard L., Nancy M. Frick, Susan Creange, Jerald R. Zimmerman, and Todd Lewis. "Polioencephalitis and the Brain Fatigue Generator Model of Post-Viral Fatigue Syndromes." Journal of Chronic Fatigue Syndrome 2, no. 2-3 (January 1996): 5–27. http://dx.doi.org/10.1300/j092v02n02_02.

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McDermott, Mark R., Chris Bendle, Murray Griffin, and Adrian Furnham. "Does It Matter What You Call It? Lay Beliefs for Overcoming Chronic Fatigue Syndrome, Myalgic Encephalomyelitis, and Post-Viral Fatigue Syndrome." Ethical Human Psychology and Psychiatry 18, no. 2 (2016): 150–62. http://dx.doi.org/10.1891/1559-4343.18.2.150.

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The study reported here examines variation in beliefs about how best to overcome a health complaint when it is nominally designated in one of 3 different ways, namely, as chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME), or as post-viral fatigue syndrome (PVFS). In a repeated measures design, the participant sample (n= 140) was presented with an adapted version of Knapp and Karabenick’s (1985) questionnaire which asks respondents to rate the degree to which single-item coping strategies would be most useful for overcoming each of the 3 designated complaints. Factor analysis of the coping items produces 3 groups of items as belief components: “self-reliance,” “seeking help,” and “external control.” The chronic fatigue syndrome appellation invoked significantly higher scores on the self-reliance factor and on external control than did the other two diagnostic labels. However, seeking help was considered to be the most important strategy for overcoming all three of the designated incarnations of the condition. In conclusion, “chronic fatigue syndrome” is the linguistic construction that bestows the most beneficial outlook for assisting individuals to overcome this complaint. Thereby, the use of this descriptor in current medical nomenclatures arguably is well placed.

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Preedy, V. R., D. G. Smith, J. R. Salisbury, and T. J. Peters. "Biochemical and muscle studies in patients with acute onset post-viral fatigue syndrome." Journal of Clinical Pathology 46, no. 8 (August 1, 1993): 722–26. http://dx.doi.org/10.1136/jcp.46.8.722.

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Jamal, Goran A., and Stig Hansen. "Post-Viral Fatigue Syndrome: Evidence for Underlying Organic Disturbance in the Muscle Fibre." European Neurology 29, no. 5 (1989): 273–76. http://dx.doi.org/10.1159/000116426.

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30

MORRISON, L. J. A., W. H. M. BEHAN, and P. O. BEHAN. "Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome." Clinical & Experimental Immunology 83, no. 3 (June 28, 2008): 441–46. http://dx.doi.org/10.1111/j.1365-2249.1991.tb05658.x.

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31

Lyons, D., M. Frampton, S. Naqvi, D. Donohoe, G. Adams, and K. Glynn. "Fallout from the COVID-19 pandemic – should we prepare for a tsunami of post viral depression?" Irish Journal of Psychological Medicine 37, no. 4 (May 15, 2020): 295–300. http://dx.doi.org/10.1017/ipm.2020.40.

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The current COVID-19 pandemic is not just a medical and social tragedy, but within the threat of the outbreak looms the potential for a significant and persistent negative mental health impact, based on previous experience with other pandemics such as Severe Acute Respiratory Syndrome (SARS) in 2003 and the earlier H1N1 outbreak of 1918. This piece will highlight the links between depression and viral illnesses and explore important overlaps with myalgic encephalomyelitis/chronic fatigue syndrome, potentially implicating inflammatory mechanisms in those exposed to a range of viral agents. While containment of psychological distress currently focuses on social anxiety and quarantine measures, a second wave of psychological morbidity due to viral illness may be imminent.

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Araja, D., U. Berkis, A. Lunga, and M. Murovska. "PMU29 Burden of COVID-19 Consequences: an Example of Post-viral Chronic Fatigue Syndrome." Value in Health 24 (June 2021): S149—S150. http://dx.doi.org/10.1016/j.jval.2021.04.741.

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33

Thadchanamoorthy, Vijayakumary, and Kavinda Dayasiri. "Postdengue chronic fatigue syndrome in an adolescent boy." BMJ Case Reports 14, no. 6 (June 2021): e238605. http://dx.doi.org/10.1136/bcr-2020-238605.

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Chronic fatigue syndrome (CFS) is often preceded by a viral illness and has recurrent ‘flulike’ symptoms which include a wide spectrum of musculoskeletal and neurological clinical features. The condition is also known as myalgic encephalomyelitis and systemic exertional intolerance syndrome. CFS has been reported following dengue among adult patients. We report the case of an 11-year-old boy who developed CFS following recovery of dengue haemorrhagic fever (DHF). The reported child was initially managed as for DHF and was clinically asymptomatic on post-discharge day 3. He was re-admitted after 3 weeks with severe joint pains, myalgia and unbearable headache. As his symptoms persisted, he was investigated in-depth. All investigations were normal except mild elevation of liver functions. The diagnosis of CFS secondary to DHF was made by exclusion of differential diagnosis. At 1-year follow-up, patient continues to have symptoms after treatment with physiotherapy and nutrition counselling.

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Cope, Helen, Amanda Pernet, Brian Kendall, and Anthony David. "Cognitive Functioning and Magnetic Resonance Imaging in Chronic Fatigue." British Journal of Psychiatry 167, no. 1 (July 1995): 86–94. http://dx.doi.org/10.1192/bjp.167.1.86.

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BackgroundThis study examines whether cognitive dysfunction in chronic fatigue may be accounted for by depression and anxiety or is due to brain pathology evident on magnetic resonance imaging (MRI).MethodTwenty-six subjects with chronic fatigue, with and without coexisting depression, and 18 age-matched normal controls were recruited from primary care following a presumed viral illness six months previously. Comparison was made with 13 psychiatric controls with depressive illness on standardised cognitive tests. MRI determined the presence of cerebral white-matter lesions.ResultsNo substantial differences in performance were shown between subjects with chronic fatigue, most of whom met the criteria for chronic fatigue syndrome, and controls. Subjective cognitive dysfunction increased with psychopathology. White-matter lesions were found in a minority from all groups. Improvement in fatigue and depression coincided with improved performance on cognitive measures.ConclusionsSubjective complaints of cognitive impairment are a prominent feature of chronic fatigue, but objective cognitive and MRI abnormalities are not. Such complaints probably reflect psychopathology rather than a post-viral process.

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Hickie, Ian, Tracey Davenport, Denis Wakefield, Ute Vollmer-Conna, Barbara Cameron, Suzanne D. Vernon, William C. Reeves, and Andrew Lloyd. "Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study." BMJ 333, no. 7568 (September 1, 2006): 575. http://dx.doi.org/10.1136/bmj.38933.585764.ae.

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Teahon, K., V. R. Preedy, D. G. Smith, and T. J. Peters. "Clinical Studies of the Post-Viral Fatigue Syndrome (PVFS) with Special Reference to Skeletal Muscle Function." Clinical Science 75, s19 (December 1, 1988): 45P. http://dx.doi.org/10.1042/cs075045pa.

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Gray, J. B., A. B. Bridges, and G. P. McNeill. "Atrial Myxoma: A Rare Cause of Progressive Exertional Dyspnoea." Scottish Medical Journal 37, no. 6 (December 1992): 186–87. http://dx.doi.org/10.1177/003693309203700609.

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A 40 year old man suffered eight years of vague but disabling symptoms, initially thought to be related to post viral fatigue syndrome, but ameliorated by the removal of a large atrial myxoma. The diagnosis of atrial myxoma is notoriously difficult, but should be excluded by echocardiography if there are predominant symptoms of progressive exertional dyspnoea, even in the absence of cardiological signs.

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Bouza, Emilio, Rafael Cantón Moreno, Pilar De Lucas Ramos, Alejandra García-Botella, Alberto García-Lledó, Javier Gómez-Pavón, Juan González del Castillo, et al. "Post-COVID syndrome: A reflection and opinion paper." Revista Española de Quimioterapia 34, no. 4 (April 20, 2021): 269–79. http://dx.doi.org/10.37201/req/023.2021.

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A high proportion of people who have suffered from COVID-19 report, after recovery from the acute phase of the disease, clinical manifestations, both subjective and objective, that continue beyond 3 weeks or even 3 months after the original clinical disease. There is still no agreed nomenclature to refer to this condition, but perhaps the most commonly used is post-COVID syndrome. The Scientific Committee on COVID of the Madrid College of Physicians (ICOMEM) has discussed this problem with a multidisciplinary approach in which internists, infectious disease specialists, psychiatrists, pneumologists, surgeons, geriatricians, pediatricians, microbiologists, family physicians and other specialists have participated, trying to gather the existing information and discussing it in the group. The clinical manifestations are very variable and range from simple fatigue to persistent fibrosing lung lesions with objective alterations of pulmonary function. Post-COVID syndrome seems to be particularly frequent and severe in adults who have required admission to Intensive Care Units and has a peculiar behavior in a very small group of children. The post-COVID syndrome, which undoubtedly exists, is at first sight not clearly distinguishable from clinical manifestations that which occur after other acute viral diseases and after prolonged stays in ICUs due to other diseases. Therefore, it offers excellent research opportunities to clarify its pathogenesis and possibly that of other related entities. It is possible that progressively there will be an increased demand for care among the millions of people who have suffered and overcome acute COVID for which the health authorities should design mechanisms for the agile management of care that will possibly require well-coordinated multidisciplinary groups. This paper, structured in questions on different aspects of the post-COVID syndrome, attempts to stage the current state of this problem

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Poenaru, Sonia, Sara J. Abdallah, Vicente Corrales-Medina, and Juthaporn Cowan. "COVID-19 and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review." Therapeutic Advances in Infectious Disease 8 (January 2021): 204993612110093. http://dx.doi.org/10.1177/20499361211009385.

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Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection. A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings. The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses. There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.

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Hayden, Melvin R. "Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID." Neuroglia 2, no. 1 (August 30, 2021): 7–35. http://dx.doi.org/10.3390/neuroglia2010004.

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The COVID-19 pandemic has paralleled the great Spanish flu pandemic of 1918–1919 in the United States. Previous historical accounts have strongly suggested a post-viral syndrome and, currently, a post-COVID-19 viral syndrome is unquestionable, which shares many of the characteristics of myalgic encephalomyelitis/chronic fatigue syndrome that is present globally. The original term for this post-acute sequela of SARS-CoV-2 (PASC) was termed long haulers by those who were affected with this syndrome and it is now termed long COVID (LC) or PASC. International researchers and clinicians are desperately trying to better understand the pathobiological mechanisms possibly involved in this syndrome. This review aims to summarize many of the cumulated findings associated with LC/PASC and provides supportive and representative illustrations and transmission electron micrographic remodeling changes within brain tissues associated with a stress type of injury as occurs in the classic db/db and novel BTBR ob/ob obesity and diabetes mellitus mice models. These models are utilized to merely provide a response to metabolic stress injury wound healing mechanisms that are also present in humans. This review posits that neuroglial activation and chronic neuroinflammation may be a common denominator for the development of the complex LC/PASC syndrome following acute COVID-19 due to SARS-CoV-2.

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Mahmud, Reaz, Md Mujibur Rahman, Mohammad Aftab Rassel, Farhana Binte Monayem, S. K. Jakaria Been Sayeed, Md Shahidul Islam, and Mohammed Monirul Islam. "Post-COVID-19 syndrome among symptomatic COVID-19 patients: A prospective cohort study in a tertiary care center of Bangladesh." PLOS ONE 16, no. 4 (April 8, 2021): e0249644. http://dx.doi.org/10.1371/journal.pone.0249644.

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Background Post-coronavirus disease (COVID-19) syndrome includes persistence of symptoms beyond viral clearance and fresh development of symptoms or exaggeration of chronic diseases within a month after initial clinical and virological cure of the disease with a viral etiology. We aimed to determine the incidence, association, and risk factors associated with development of the post-COVID-19 syndrome. Methods We conducted a prospective cohort study at Dhaka Medical College Hospital between June 01, 2020 and August 10, 2020. All the enrolled patients were followed up for a month after clinical improvement, which was defined according the World Health Organization and Bangladesh guidelines as normal body temperature for successive 3 days, significant improvement in respiratory symptoms (respiratory rate <25/breath/minute with no dyspnea), and oxygen saturation >93% without assisted oxygen inhalation. Findings Among the 400 recruited patients, 355 patients were analyzed. In total, 46% patients developed post-COVID-19 symptoms, with post-viral fatigue being the most prevalent symptom in 70% cases. The post-COVID-19 syndrome was associated with female gender (relative risk [RR]: 1.2, 95% confidence interval [CI]: 1.02–1.48, p = 0.03), those who required a prolonged time for clinical improvement (p<0.001), and those showing COVID-19 positivity after 14 days (RR: 1.09, 95% CI: 1.00–1.19, p<0.001) of initial positivity. Patients with severe COVID-19 at presentation developed post-COVID-19 syndrome (p = 0.02). Patients with fever (RR: 1.5, 95% CI: 1.05–2.27, p = 0.03), cough (RR: 1.36, 95% CI: 1.02–1.81, p = 0.04), respiratory distress (RR: 1.3, 95% CI: 1.4–1.56, p = 0.001), and lethargy (RR: 1.2, 95% CI: 1.06–1.35, p = 0.003) as the presenting features were associated with the development of the more susceptible to develop post COVID-19 syndrome than the others. Logistic regression analysis revealed female sex, respiratory distress, lethargy, and long duration of the disease as risk factors. Conclusion Female sex, respiratory distress, lethargy, and long disease duration are critical risk factors for the development of post-COVID-19 syndrome.

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White, P. D. "Post-Viral Fatigue Syndrome. Edited by R. Jenkins and J. Mowbray. (Pp. 463; illustrated; £60.00.) John Wiley: Chichester. 1991." Psychological Medicine 22, no. 3 (August 1992): 817–19. http://dx.doi.org/10.1017/s0033291700038277.

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Layzer, Robert B. "Post-viral fatigue syndrome. Edited by Rachel Jenkins and James F. Mowbray, Chichester, John Wiley, 1991, 463 pp, $137.50." Annals of Neurology 35, no. 2 (February 1994): 250–52. http://dx.doi.org/10.1002/ana.410350233.

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Pfeffer, Jeremy M. "Post-Viral Fatigue Syndrome. Edited by Rachel Jenkins and James Mowbray. Chichester: John Wiley & Sons. 463 pp. £60.00." British Journal of Psychiatry 160, no. 4 (April 1992): 581. http://dx.doi.org/10.1192/s000712500003703x.

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King, David J., and Stephen J. Cooper. "Viruses, Immunity and Mental Disorder." British Journal of Psychiatry 154, no. 1 (January 1989): 1–7. http://dx.doi.org/10.1192/bjp.154.1.1.

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Are viruses the cause of mental illness, or does stress or mental disorder produce impaired immunity, with increased susceptibility to infection? These two separate but not unrelated questions have been debated periodically and there has been much renewed interest recently, with increased sophistication in immunology and widespread topical concern about immunodeficiency. The neuropsychiatry of the acquired immunodeficiency syndrome (AIDS) (Snider et al, 1983; Carne & Adler, 1986; Wortis, 1986; Burton, 1987; Fenton, 1987) and the validity of a ‘post-viral fatigue syndrome’ as a clinical entity (Behan, 1983; Southern & Oldstone, 1986; Dawson, 1987; David et al, 1988) are not discussed here, but have been dealt with in the editorials and reviews cited.

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Ebzeeva, E. Yu, O. D. Ostroumova, and E. V. Mironova. "Efficacy and safety of Mildronate in treatment of postinfectious asthenic syndrome (clinical examples)." Medical alphabet, no. 2 (June 12, 2020): 61–66. http://dx.doi.org/10.33667/2078-5631-2020-2-61-66.

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Asthenic syndrome is a non‑specific syndrome that is often found in general medical practice in patients with various somatic pathologies both during an exacerbation of a chronic disease, and after an acute process. The leading symptoms in the clinic of asthenia are pathological weakness and fatigue. According to various researchers, they are found in 15–45 % of people. To date, there is no universally accepted definition and clear classification of this syndrome. The main pathogenetic concepts are the psychosocial, infectious‑immune theory of asthenia. The development of asthenic syndrome in patients with somatic pathology may be associated with the depletion of the functional capabilities of the nervous system due to disturbances in the blood supply to the brain, auto‑toxicity or exposure to exogenous toxic factors in bacterial, viral infections. There is no specific treatment for this condition. This article presents two clinical cases of the development of post‑infection asthenic syndrome in a 47‑year‑old patient against community‑acquired pneumonia and in a 36‑year‑old patient after an acute respiratory‑viral infection of moderate severity. In both cases, drug treatment with Mildronate was carried out with a positive trend in the form of regression of asthenia symptoms, side effects during treatment. Mildronate belongs to the class of cytoprotectors – antihypoxants, activates glycolysis and prevents impaired transport of adenosine triphosphate, providing a sufficient level of energy synthesis, which allows cells to maintain homeostasis and morphological integrity. The immunoadjuvant properties of Mildronate are very important in post‑infectious asthenic syndrome, since a violation of the immune response plays a central role in its pathogenesis. The immunoadjuvant properties of Mildronate have been discovered in a number of studies.

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47

Tuormaa, Tuula E. "A Brief Review of the Immune System and its Function in Relation to: PVFS, Non-Antibody Mediated Allergy, Autoimmunity and Immune Deficiency." Nutrition and Health 6, no. 1 (January 1988): 53–62. http://dx.doi.org/10.1177/026010608800600105.

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This paper comprises a short summary of the immune system function with particular emphasis on the red blood cells' function in immunity. The basic biochemical features of Post Viral Fatique Syndrome, Non-Antibody mediated Allergy, Autoimmunity and Immune deficiency is described and treatment procedure using Nutritional Medicine suggested.

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Wei, Kai-Che, Wan-Ju Wei, Yi-Shan Liu, Li-Chen Yen, and Tsung-Hsien Chang. "Assessment of Prolonged Dengue Virus Infection in Dermal Fibroblasts and Hair-Follicle Dermal Papilla Cells." Viruses 12, no. 3 (February 28, 2020): 267. http://dx.doi.org/10.3390/v12030267.

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Dengue virus (DENV)-mediated hair loss is one of the post-dengue fatigue syndromes and its pathophysiology remains unknown. Whether long-term or persistent infection with DENV in the scalp results in hair loss is unclear. In this study, we cultured human dermal fibroblasts (WS1 cells) and primary human hair-follicle dermal papilla cells (HFDPCs) in the long term with DENV-2 infection. The production of virion, the expression of inflammatory and anti-virus genes, and their signaling transduction activity in the infected cells were analyzed. DENV-2 NS3 protein and DENV-2 5′ UTR RNA were detected in fibroblasts and HFDPCs that were subjected to long-term infection with DENV-2 for 33 days. A significant amount of DENV-2 virion was produced by both WS1 cells and HFDPCs in the first two days of acute infection. The virion was also detected in WS1 cells that were infected in the long term, but HFDPCs failed to produce DENV-2 after long-term culture. Type I and type III interferons, and inflammatory cytokines were highly expressed in the acute phase of DENV infection in HFPDC and WS1 cells. However, in the long-term cultured cells, modest levels of anti-viral protein genes were expressed and we observed reduced signaling activity, which was correlated with the level of virus production changes. Long-term infection of DENV-2 downregulated the expression of hair growth regulatory factors, such as Rip1, Wnt1, and Wnt4. This in vitro study shows that the long-term infection with DENV-2 in dermal fibroblasts and dermal papilla cells may be involved with the prolonged-DENV-infection-mediated hair loss of post-dengue fatigue syndrome. However, direct evidence for viral replication in the human hair of a dengue victim or animal infection model is required.

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Williams, Leah R., and Carol Isaacson-Barash. "Three Cases of Severe ME/CFS in Adults." Healthcare 9, no. 2 (February 16, 2021): 215. http://dx.doi.org/10.3390/healthcare9020215.

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex, only partially understood multi-system disease whose onset and severity vary widely. Symptoms include overwhelming fatigue, post-exertional malaise, sleep disruptions, gastrointestinal issues, headaches, orthostatic intolerance, cognitive impairment, etc. ME/CFS is a physiological disease with an onset often triggered by a viral or bacterial infection, and sometimes by toxins. Some patients have a mild case and are able to function nearly on a par with healthy individuals, while others are moderately ill and still others are severely, or even, very severely ill. The cohort of moderately to very severely ill is often housebound or bedbound, has lost employment or career, and has engaged in a long, and often futile, search for treatment and relief. Here, we present three case studies, one each of a moderately ill, a severely ill, and a very severely ill person, to demonstrate the complexity of the disease, the suffering of these patients, and what health care providers can do to help.

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Araja, Diana, Uldis Berkis, Asja Lunga, and Modra Murovska. "Shadow Burden of Undiagnosed Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) on Society: Retrospective and Prospective—In Light of COVID-19." Journal of Clinical Medicine 10, no. 14 (July 6, 2021): 3017. http://dx.doi.org/10.3390/jcm10143017.

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Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a poorly understood, complex, multisystem disorder, with severe fatigue not alleviated by rest, and other symptoms, which lead to substantial reductions in functional activity and quality of life. Due to the unclear aetiology, treatment of patients is complicated, but one of the initial problems is the insufficient diagnostic process. The increase in the number of undiagnosed ME/CFS patients became specifically relevant in the light of the COVID-19 pandemic. The aim of this research was to investigate the issues of undiagnosed potential ME/CFS patients, with a hypothetical forecast of the expansion of post-viral CFS as a consequence of COVID-19 and its burden on society. Methods: The theoretical research was founded on the estimation of classic factors presumably affecting the diagnostic scope of ME/CFS and their ascription to Latvian circumstances, as well as a literature review to assess the potential interaction between ME/CFS and COVID-19 as a new contributing agent. The empirical study design consisted of two parts: The first part was dedicated to a comparison of the self-reported data of ME/CFS patients with those of persons experiencing symptoms similar to ME/CFS, but without a diagnosis. This part envisaged the creation of an assumption of the ME/CFS shadow burden “status quo”, not addressing the impact of COVID-19. The second part aimed to investigate data from former COVID-19 patients’ surveys on the presence of ME/CFS symptoms, 6 months after being affected by COVID-19. Descriptive and analytical statistical methods were used to analyse the obtained data. Results: The received data assumed that the previously obtained data on the ME/CFS prevalence of 0.8% in the Latvian population are appropriate, and the literature review reports a prevalence of 0.2–1.0% in developed countries. Regarding the reciprocity of ME/CFS and COVID-19, the literature review showed a lack of research in this field. The empirical results show quite similar self-esteem among ME/CFS patients and undiagnosed patients with longstanding disease experience, while former COVID-19 patients show a significantly lower severity of these problems. Notably, “psychological distress (anxiety)” and “episodic fatigue” are significantly predominant symptoms reported by former COVID-19 patients in comparison with ME/CFS patients and undiagnosed patients prior to the COVID-19 pandemic. The results of our analysis predict that the total amount of direct medical costs for undiagnosed patients (out-of-pocket payments) is more than EUR 15 million p.a. (in Latvia), and this may increase by at least 15% due to the consequences of COVID-19. Conclusions: ME/CFS creates a significant shadow burden on society, even considering only the direct medical costs of undiagnosed patients—the number of whom in Latvia is probably at least five times higher than the number of discerned patients. Simultaneously, COVID-19 can induce long-lasting complications and chronic conditions, such as post-viral CFS, and increase this burden. The Latvian research data assume that ME/CFS patients are not a high-risk group for COVID-19; however, COVID-19 causes ME/CFS-relevant symptoms in patients. This increases the need for monitoring of patients for even longer after recovering from COVID-19′s symptoms, in order to prevent complications and the progression of chronic diseases. In the context of further epidemiological uncertainty, and the possibility of severe post-viral consequences, preventive measures are becoming significantly more important; an integrated diagnostic approach and appropriate treatment could reduce this burden in the future.

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Journal articles on the topic 'Post Viral Fatigue Syndrome'

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