scholarly journals Can persistent Epstein–Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?

2012 ◽  
Vol 6 (2) ◽  
pp. 740-762 ◽  
Author(s):  
Elena Agliari ◽  
Adriano Barra ◽  
Kristian Gervasi Vidal ◽  
Francesco Guerra
Author(s):  
Michael Sharpe ◽  
Simon Wessely

Chronic fatigue syndrome is a controversial condition, conflicts about which have frequently burst out of the medical literature into the popular media. Whilst these controversies may initially seem to be of limited interest to those who do not routinely treat such patients, they also exemplify important current issues in medicine. These issues include the nature of symptom-defined illness; patient power versus medical authority; and the uncomfortable but important issues of psychological iatrogenesis. The subject is therefore of relevance to all doctors. Fatigue is a subjective feeling of weariness, lack of energy, and exhaustion. Approximately 20 per cent of the general population report significant and persistent fatigue, although relatively few of these people regard themselves as ill and only a small minority seek a medical opinion. Even so, fatigue is a common clinical presentation in primary care. When fatigue becomes chronic and associated with disability it is regarded as an illness. Such a syndrome has been recognized at least since the latter half of the last century. Whilst during the Victorian era patients who went to see doctors with this illness often received a diagnosis of neurasthenia, a condition ascribed to the effect of the stresses of modern life on the human nervous system the popularity of this diagnosis waned and by the mid-twentieth century it was rarely diagnosed (although the diagnosis subsequently became popular in the Far East—see Chapter 5.2.1). Although it is possible that the prevalence of chronic fatigue had waned in the population, it is more likely that patients who presented in this way were being given alternative diagnoses. These were mainly the new psychiatric syndromes of depression and anxiety, but also other labels indicating more direct physical explanations, such as chronic brucellosis, spontaneous hypoglycaemia, and latterly chronic Epstein–Barr virus infection. As well as these sporadic cases of fatiguing illness, epidemics of similar illnesses have been occasionally reported. One which occurred among staff at the Royal Free Hospital, London in 1955 gave rise to the term myalgic encephalomyelitis (ME), although it should be emphasized that the nature and symptoms of that outbreak are dissimilar to the majority of those now presenting to general practitioners under the same label. A group of virologists and immunologists proposed the term chronic fatigue syndrome in the late 1980s. This new and aetiologically neutral term was chosen because it was increasingly recognized that many cases of fatigue were often not readily explained either by medical conditions such as Epstein–Barr virus infection or by obvious depression and anxiety disorders. Chronic fatigue syndrome has remained the most commonly used term by researchers. The issue of the name is still not completely resolved however: Neurasthenia remains in the ICD-10 psychiatric classification as a fatigue syndrome unexplained by depressive or anxiety disorder, whilst the equivalent in DSM-IV is undifferentiated somatoform disorder. Myalgic encephalomyelitis or (encephalopathy) is in the neurological section of ICD-10 and is used by some to imply that the illness is neurological as opposed to a psychiatric one. Unfortunately the case descriptions under these different labels make it clear that they all reflect similar symptomatic presentations, adding to confusion. Official UK documents have increasingly adopted the uneasy and probably ultimately unsatisfactory compromise term CFS/ME. In this chapter, we will use the simple term chronic fatigue syndrome (CFS).


1996 ◽  
Vol 28 (2) ◽  
pp. 185-187 ◽  
Author(s):  
Antonio López Navidad ◽  
Pere Domingo ◽  
Juan C. López Talavera ◽  
Nuria Rabella ◽  
Guillem Verger

In article presented results of the study of basic levels of regulatory cytokines in patients with various forms of Epstein-Barr virus infection. Analysis of the dynamics of cytokine profile in patients with Epstein-Barr virus infection revealed the opposite changes studied synthesis of proinflammatory and anti-inflammatory cytokines, which was the basis for the establishment of the four types of immune response. The findings confirm the existence of cytokine imbalance with Epstein-Barr virus infection. The established types of immune responses indicate inadequate cell humoral reactivity in a long persistence of Epstein-Barr virus infection, which manifests a tendency to suppression of cell-mediated and humoral immune response enhancement mechanisms and displayed in the clinical and biochemical manifestations of the disease, and also leads to prolonged undulating course. The results of studies confirm the existence of cytokine imbalance in various forms of EBV infection. The established types of immune response indicate inadequate cellular-humoral reactivity of the organism under the conditions of long-term EBV persistence. This is manifested by a tendency to suppress cell-mediated and increased humoral mechanisms of the immune response and is displayed in the clinical and biochemical manifestations of the disease and leads to a prolonged wave-like course of the disease. Interesting and promising are studies aimed at the medical correction of identified disorders in established types of immune response in patients with HEVE and studying the effects of the latter on the outcomes of the disease, the development of complications and activity of the process, which will be the subject of our further study.


2019 ◽  
Vol 75 ◽  
pp. 94-100 ◽  
Author(s):  
Maria Pedersen ◽  
Tarjei Tørre Asprusten ◽  
Kristin Godang ◽  
Truls Michael Leegaard ◽  
Liv Toril Osnes ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Youwei Lu ◽  
Xi Zhang ◽  
Wei Hu ◽  
Qianhong Yang

Background. Atherosclerosis (AS) is a type of yellow substance containing cholesterol in the intima of large and middle arteries, which is mostly caused by fat metabolism disorders and neurovascular dysfunction. Materials and Methods. The GSE100927 data got analyzed to find out the differentially expressed genes (DEGs) using the limma package in R software. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of the DEGs were assessed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The Search Tool for the Retrieval of Interacting Genes (STRING) visualized the Protein-Protein Interaction (PPI) network of the aggregated DEGs. GSEA software was used to verify the biological process. Result. We screened 1574 DEGs from 69 groups of atherosclerotic carotid artery and 35 groups of control carotid artery, including 1033 upregulated DEGs and 541 downregulated DEGs. DEGs of AS were chiefly related to immune response, Epstein-Barr virus infection, vascular smooth muscle contraction, and cGMP-PKG signaling pathway. Through PPI networks, we found that the hub genes of AS were PTAFR, VAMP8, RNF19A, VPRBP, RNF217, KLHL42, NEDD4, SH3RF1, UBE2N, PJA2, RNF115, ITCH, SKP1, FBXW4, and UBE2H. GSEA analysis showed that GSE100927 was concentrated in RIPK1-mediated regulated necrosis, FC epsilon receptor fceri signaling, Fceri-mediated NF KB activation, TBC rabgaps, TRAF6-mediated induction of TAK1 complex within TLR4 complex, and RAB regulation of trafficking. Conclusion. Our analysis reveals that immune response, Epstein-Barr virus infection, and so on were major signatures of AS. PTAFR, VAMP8, VPRBP, RNF217, KLHL42, and NEDD4 might facilitate the AS tumorigenesis, which could be new biomarkers for diagnosis and therapy of AS.


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