Long COVID, in which disease-related symptoms persist for months after recovery, has led to a revival of the discussion of whether neuropsychiatric long-term symptoms after viral infections indeed result from virulent activity or are purely psychological phenomena. In this review, we demonstrate that, despite showing differences in structure and targeting, many viruses have highly similar neuropsychiatric effects on the host. Herein, we compare severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human immunodeficiency virus 1 (HIV-1), Ebola virus disease (EVD), and herpes simplex virus 1 (HSV-1). We provide evidence that the mutual symptoms of acute and long-term anxiety, depression and post-traumatic stress among these viral infections are likely to result from primary viral activity, thus suggesting that these viruses share neuroinvasive strategies in common. Moreover, it appears that secondary induced environmental stress can lead to the emergence of psychopathologies and increased susceptibility to viral (re)infection in infected individuals. We hypothesize that a positive feedback loop of virus-environment-reinforced systemic responses exists. It is surmised that this cycle of primary virulent activity and secondary stress-induced reactivation, may be detrimental to infected individuals by maintaining and reinforcing the host's immunocompromised state of chronic inflammation, immunological strain, and maladaptive central-nervous-system activity. We propose that this state can lead to perturbed cognitive processing and promote aversive learning, which may manifest as acute, long-term neuropsychiatric illness.

• Klíčová slova
• HIV-1, SARS virus, interoception, neuropsychiatry, virus latency,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Mitochondrial DNA (mtDNA) heteroplasmy is the dynamically determined co-expression of wild type (WT) inherited polymorphisms and collective time-dependent somatic mutations within individual mtDNA genomes. The temporal expression and distribution of cell-specific and tissue-specific mtDNA heteroplasmy in healthy individuals may be functionally associated with intracellular mitochondrial signaling pathways and nuclear DNA gene expression. The maintenance of endogenously regulated tissue-specific copy numbers of heteroplasmic mtDNA may represent a sensitive biomarker of homeostasis of mitochondrial dynamics, metabolic integrity, and immune competence. Myeloid cells, monocytes, macrophages, and antigen-presenting dendritic cells undergo programmed changes in mitochondrial metabolism according to innate and adaptive immunological processes. In the central nervous system (CNS), the polarization of activated microglial cells is dependent on strategically programmed changes in mitochondrial function. Therefore, variations in heteroplasmic mtDNA copy numbers may have functional consequences in metabolically competent mitochondria in innate and adaptive immune processes involving the CNS. Recently, altered mitochondrial function has been demonstrated in the progression of coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Accordingly, our review is organized to present convergent lines of empirical evidence that potentially link expression of mtDNA heteroplasmy by functionally interactive CNS cell types to the extent and severity of acute and chronic post-COVID-19 neurological disorders.

• Klíčová slova
• COVID-19, Central nervous system, Gut microbiome, Immune response, Mitochondrial DNA, SARS-CoV-2,
• MeSH
• COVID-19 komplikace   genetika   imunologie   metabolismus   MeSH
• heteroplazmie genetika   MeSH
• imunita MeSH
• lidé MeSH
• mitochondriální DNA genetika   MeSH
• mitochondrie metabolismus   MeSH
• nemoci nervového systému komplikace   genetika   imunologie   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• mitochondriální DNA MeSH

During the COVID-19 pandemic, research on the relationships between the virus and its human host has become fundamental to understand this pathology and its effects. Attaining this profound understanding is critical for the effective containment and treatment of infections caused by the virus. In this review, we present some possible mechanisms by which psychopathological symptoms emerge following viral infections of the central nervous system (CNS). These proposed mechanisms are based on microbial communication and the induced priming of microglial antibody activation within the CNS through Toll-like receptor signaling. In this process, chronic microglial activation causes increased glutamate release in virally-altered, high-density neuronal structures, thereby modulating cognitive networks and information integration processes. This modulation, in turn, we suggest, affects the accuracy of sensory integration and connectivity of major control networks, such as the default mode network. The chronic activation of immunological responses and neurochemical shifts toward an elevated glutamate/gamma-aminobutyric acid ratio lead to negative reinforcement learning and suboptimal organismic functioning, for example, maintaining the body in an anxious state, which can later become internalized as trait anxiety. Therefore, we hypothesize that the homeostatic relationship between host, microbiome, and virome, would be decisive in determining the efficiency of subsequent immunological responses, disease susceptibility, and long-term psychopathological effects of diseases that impact the CNS, such as the COVID-19.

• Klíčová slova
• COVID-19, anxiety disorders, brain, cognition, default mode network, glutamic acid, immunity, microbiota,
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Trait anxiety is characterized as a constant and often subliminal state that persists during daily life. Interoception is the perception of internal states and sensations, including from the autonomic nervous system. This review aims to develop a predictive model to explain the emergence, manifestations, and maintenance of trait anxiety. The model begins with the assumption that anxiety states arise from active interoceptive inference. The subsequent activation of autonomic responses results from aversive sensory encounters. A cognitive model is proposed for trait anxiety that includes the aversive sensory components from interoception, exteroception, and proprioception. A further component of the hypothesis is that repeated exposure to subliminal anxiety-evoking sensory elements can lead to an overgeneralization of this response to other inputs that are generally non-aversive. Increased uncertainty may result when predicting the sensory environment, resulting in arbitrary interoceptive anxiety responses that may be due to unjustifiable causes. Arbitrary successful or unsuccessful matching of predictions and responses reduces the individual's confidence to maintain the anxiety trait. In this review, the application of the proposed model is illustrated using gut microbial dysbiosis or imbalance of the gut microbiome.

• MeSH
• dysbióza patofyziologie   MeSH
• interocepce fyziologie   MeSH
• kognice fyziologie   MeSH
• lidé MeSH
• střevní mikroflóra fyziologie   MeSH
• úzkost patofyziologie   MeSH
• úzkostné poruchy patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Anthropogenic environmental pollutants affect many physiological, biochemical, and endocrine actions as reproduction, metabolism, immunity, behavior and as such can interfere with any aspect of hormone action. Microbiota and their genes, microbiome, a large body of microorganisms, first of all bacteria and co-existing in the host´s gut, are now believed to be autonomous endocrine organ, participating at overall endocrine, neuroendocrine and immunoendocrine regulations. While an extensive literature is available on the physiological and pathological aspects of both players, information about their mutual relationships is scarce. In the review we attempted to show various examples where both, endocrine disruptors and microbiota are meeting and can act cooperatively or in opposition and to show the mechanism, if known, staying behind these actions.

• MeSH
• endokrinní disruptory farmakologie   MeSH
• fyziologie bakterií účinky léků   MeSH
• gastrointestinální trakt účinky léků   mikrobiologie   MeSH
• látky znečišťující životní prostředí farmakologie   MeSH
• lidé MeSH
• střevní mikroflóra účinky léků   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• endokrinní disruptory MeSH
• látky znečišťující životní prostředí MeSH

The relaxation response derives its health benefits by reestablishing "normal" equilibria between the sympathetic and parasympathetic branches of the autonomic nervous system. Recent work suggests that this behavioral training provides positive effects on mitochondrial bioenergetics, insulin secretion, and reductions in pro-inflammatory and stress-related pathways. We have previously contended, however, that correlative associations of relaxation training with positive changes in gene expression in selected biological systems are strongly suggestive of adaptive physiological changes, but do not elucidate an underlying, clinically compelling, unified mechanism of action consistent with its purported positive health effects. We surmise that any plausible model of behaviorally-mediated regulatory effects on whole-body metabolic processes must be intrinsically broad-based and multifaceted via integration of differential contributions of functionally interactive peripheral and CNS organ systems. Accordingly, the initiation of multiple cellular protective/anti-bio-senescence processes may have emerged during evolutionary development to ensure the survival of hybrid prokaryotic/eukaryotic progenitor cells, given the evolvement of oxidative metabolism and its associated negative byproducts. As an essential corollary, preservation and adaptation of multifaceted regulatory molecules, notably nitric oxide, paralleled the development of eukaryotic cell types via multifaceted stereo-selective recognition and conformational matching by complex biochemical and molecular enzyme systems. Hence, the relaxation response may be a manifestation of a metabolic corrective process/response, that may now include cognition ("awareness").

• MeSH
• adenosintrifosfát metabolismus   MeSH
• buněčné dýchání fyziologie   MeSH
• energetický metabolismus MeSH
• lidé MeSH
• mitochondrie metabolismus   fyziologie   MeSH
• oxid dusnatý metabolismus   MeSH
• relaxace fyziologie   MeSH
• spotřeba kyslíku fyziologie   MeSH
• teoretické modely MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• úvodníky MeSH
• Názvy látek
• adenosintrifosfát MeSH
• oxid dusnatý MeSH

Stress affects cellular aging and inflammatory and chromosomal processes, including telomere length, thereby potentially compromising health and facilitating disease onset and progression. Stress-related diseases and strategies to manage stress usually require integrative or behavioral therapeutic approaches that also operate on cellular levels. Mind-body medicine (MBM) uses the interaction between the mind, body, behavior, and the environment to correct physical and psychological malfunctions, thus ameliorating disease states and improving health. The relaxation response (RR) is a physiological opponent of stress and the stress response (SR) (i.e., fight-or-flight response), also invoking molecular anti-stress processes. Techniques that elicit the RR are at the core of practically all MBM interventions. We surmise that these techniques can also affect chromosomal and telomere processes, molecular aging, and the modulation of inflammatory states on cellular levels.

• MeSH
• chronická nemoc MeSH
• homeostáza telomer fyziologie   MeSH
• lidé MeSH
• psychický stres komplikace   MeSH
• psychosomatické a relaxační terapie metody   psychologie   MeSH
• relaxační terapie metody   MeSH
• stárnutí buněk fyziologie   MeSH
• stárnutí fyziologie   MeSH
• telomery fyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH