Stress-associated immune modulation: relevance to viral infections and chronic fatigue syndrome

1998 ◽  
Vol 105 (3) ◽  
pp. 35S-42S ◽  
Author(s):  
Ronald Glaser ◽  
Janice K. Kiecolt-Glaser
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Immune Modulation ◽  
Viral Infections ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

scholarly journals Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis

2021 ◽  
Vol 15 ◽  
Author(s):  
Adonis Sfera ◽  
Carolina Osorio ◽  
Carlos M. Zapata Martín del Campo ◽  
Shaniah Pereida ◽  
Steve Maurer ◽  
...  
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Viral Infections ◽  
Life Quality ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Unknown Etiology ◽  
Host Proteins ◽  
Fatigue Syndrome ◽  
Long Time ◽  
Sleep Abnormalities

Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.

scholarly journals A neuro-inflammatory model can explain the onset, symptoms and flare-ups of myalgic encephalomyelitis/chronic fatigue syndrome

2019 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Angus Mackay
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Viral Infections ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Diverse Range ◽  
Variable Threshold ◽  
Fatigue Syndrome ◽  
Neuro Inflammation

Abstract A neuro-inflammatory model is proposed to explain the onset, symptoms and perpetuation of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) via characteristic flare-ups (relapses). In this article, I explore the proposition that a range of triggers (intense physiological stressors such as severe viral infections, chemical toxin exposure or emotional trauma) in ME/CFS-predisposed people causes disruption in the neural circuitry of the hypothalamus (paraventricular nucleus), which induces a neuro-inflammatory reaction in the brain and central nervous system of ME/CFS patients, via over-active innate immune (glial) cells. Resulting dysfunction of the limbic system, the hypothalamus and consequently of the autonomic nervous system can then account for the diverse range of ME/CFS symptoms. Ongoing stressors feed into a compromised (inflamed) hypothalamus and if a certain (but variable) threshold is exceeded, a flare-up will ensue, inducing further ongoing neuro-inflammation in the central nervous system, thus perpetuating the disease indefinitely.

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