scholarly journals The COVID-19 infection in children and its association with the immune system, prenatal stress, and neurological complications

2022 ◽  
Vol 18 (2) ◽  
pp. 707-716
Author(s):  
Suliman Khan ◽  
Rabeea Siddique ◽  
Xiao Hao ◽  
Yueting Lin ◽  
Yuxin Liu ◽  
...  
2021 ◽  
Vol 13 (4) ◽  
pp. 127-132
Author(s):  
T. M. Alekseeva ◽  
P. Sh. Isabekova ◽  
M. P. Topuzova ◽  
N. V. Skripchenko

Development of various immune-mediated neurological complications after a viral infection is of particular interest to medical society during a pandemic of COVID-19. It was found that SARS-CoV-2 has the ability to cause hyperstimulation of the immune system, thereby initiating developing of autoimmune diseases. The article describes a clinical case of new onset of generalized myasthenia gravis with thymoma in a patient after previous COVID-19. 


2020 ◽  
Vol 8 (10) ◽  
pp. 1514 ◽  
Author(s):  
Carolina Ferreira ◽  
Sofia D. Viana ◽  
Flávio Reis

Coronavirus Disease 2019 (COVID-19) is a pandemic infection caused by a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients present a complex clinical picture that, in severe cases, evolves to respiratory, hepatic, gastrointestinal, and neurological complications, and eventually death. The underlying pathophysiological mechanisms are complex and multifactorial and have been summarized as a hyperresponse of the immune system that originates an inflammatory/cytokine storm. In elderly patients, particularly in those with pre-existing cardiovascular, metabolic, renal, and pulmonary disorders, the disease is particularly severe, causing prolonged hospitalization at intensive care units (ICU) and an increased mortality rate. Curiously, the same populations have been described as more prone to a gut microbiota (GM) dysbiosis profile. Intestinal microflora plays a major role in many metabolic and immune functions of the host, including to educate and strengthen the immune system to fight infections, namely of viral origin. Notably, recent studies suggest the existence of GM dysbiosis in COVID-19 patients. This review article highlights the interplay between the triad GM dysbiosis–immune hyperresponse–inflammation in the individual resilience/fragility to SARS-CoV-2 infection and presents the putative impact of pharmacological and nutraceutical approaches on the triumvirate, with focus on GM.


2014 ◽  
Vol 101-102 ◽  
pp. 41-42
Author(s):  
Greta O’Rourke ◽  
Katherina Ramisch ◽  
Khalil Karimi ◽  
Maria Emilia Solano ◽  
Petra Arck

2007 ◽  
Vol 32 (2) ◽  
pp. 114-124 ◽  
Author(s):  
Christel C.A. Vanbesien-Mailliot ◽  
Isabelle Wolowczuk ◽  
Jérôme Mairesse ◽  
Odile Viltart ◽  
Myriam Delacre ◽  
...  

2019 ◽  
Vol 19 (1S) ◽  
pp. 124-126
Author(s):  
L A Zakharova

The analysis of published and original data demonstrates that prenatal stress induced by viral and bacterial infection, or changes in the physiological concentrations of neurohormones in early ontogeny can cause unfavorable impacts on the development of neuroendocrine and immune systems. In early pregnancy bacterial infection simulated by lipopolysaccharide in an experiment activates the maternal immune system, which enhances the synthesis of pro- and anti-inflammatory cytokines in both maternal and fetal organisms. Consequently, cytokines promote the secretion of a hormonal cascade in the hypothalamic-pituitary-adrenal system, thus eliciting the hormonal response to stress. Various stress factors during critical periods of neuroendocrine and immune system development modulate the epigenetic mechanisms controlling specific genes, which can affect the structure and function of these systems and increase the risk of various pathologies in the offspring.


2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.


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