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Changes Produced by Viruses and Bacteria on the Nervous System

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 21985

Special Issue Editor

Special Issue Information

Dear Colleagues,

In the last decade, many studies on how viruses and bacteria act on the nervous system have been published. These actions produce changes in the functionality and physiology of brain cells that increase neurodegeneration and affect neurodevelopment. The pathogenesis of viral and bacterial infections is complex and involves the activation of the mononuclear phagocytic system, the release of pro-inflammatory cytokines, chemokines, and growth factors, endothelial dysfunction, alterations in the innate and adaptive immune systems, direct organ and endothelial damage from unrestrained viral and bacterial replication late in infection, and coagulopathy. We invite you to submit your latest research findings or a review article to this Special Issue, entitled “Changes Produced by Viruses and Bacteria in the Nervous System”, which we hope will bring together current research on the effects of viruses and bacteria on the nervous system. We welcome submissions concerning all aspects of changes in the nervous system produced by viruses and bacteria. We hope that this Special Issue will help highlight the most recent advances in our understanding of how viruses and bacteria act on the nervous system.

We look forward to your contribution.

Prof. Dr. Soraya L. Valles
Guest Editor

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Keywords

  • virus
  • bacteria
  • nervous system
  • inflammation
  • oxidative stress
  • endothelial dysfunction
  • innate immune system
  • adaptive immune system
  • viral and bacterial replication
  • infection

Published Papers (5 papers)

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Research

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12 pages, 3110 KiB  
Article
Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients
by Matteo Bocci, Clara Oudenaarden, Xavier Sàenz-Sardà, Joel Simrén, Arvid Edén, Jonas Sjölund, Christina Möller, Magnus Gisslén, Henrik Zetterberg, Elisabet Englund and Kristian Pietras
Int. J. Mol. Sci. 2021, 22(21), 11622; https://doi.org/10.3390/ijms222111622 - 27 Oct 2021
Cited by 42 | Viewed by 5314
Abstract
A wide range of neurological manifestations have been associated with the development of COVID-19 following SARS-CoV-2 infection. However, the etiology of the neurological symptomatology is still largely unexplored. Here, we used state-of-the-art multiplexed immunostaining of human brains (n = 6 COVID-19, median [...] Read more.
A wide range of neurological manifestations have been associated with the development of COVID-19 following SARS-CoV-2 infection. However, the etiology of the neurological symptomatology is still largely unexplored. Here, we used state-of-the-art multiplexed immunostaining of human brains (n = 6 COVID-19, median age = 69.5 years; n = 7 control, median age = 68 years) and demonstrated that expression of the SARS-CoV-2 receptor ACE2 is restricted to a subset of neurovascular pericytes. Strikingly, neurological symptoms were exclusive to, and ubiquitous in, patients that exhibited moderate to high ACE2 expression in perivascular cells. Viral dsRNA was identified in the vascular wall and paralleled by perivascular inflammation, as signified by T cell and macrophage infiltration. Furthermore, fibrinogen leakage indicated compromised integrity of the blood–brain barrier. Notably, cerebrospinal fluid from additional 16 individuals (n = 8 COVID-19, median age = 67 years; n = 8 control, median age = 69.5 years) exhibited significantly lower levels of the pericyte marker PDGFRβ in SARS-CoV-2-infected cases, indicative of disrupted pericyte homeostasis. We conclude that pericyte infection by SARS-CoV-2 underlies virus entry into the privileged central nervous system space, as well as neurological symptomatology due to perivascular inflammation and a locally compromised blood–brain barrier. Full article
(This article belongs to the Special Issue Changes Produced by Viruses and Bacteria on the Nervous System)
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17 pages, 3312 KiB  
Article
Recurrent Herpes Simplex Virus Type 1 (HSV-1) Infection Modulates Neuronal Aging Marks in In Vitro and In Vivo Models
by Giorgia Napoletani, Virginia Protto, Maria Elena Marcocci, Lucia Nencioni, Anna Teresa Palamara and Giovanna De Chiara
Int. J. Mol. Sci. 2021, 22(12), 6279; https://doi.org/10.3390/ijms22126279 - 11 Jun 2021
Cited by 14 | Viewed by 2864
Abstract
Herpes simplex virus 1 (HSV-1) is a widespread neurotropic virus establishing a life-long latent infection in neurons with periodic reactivations. Recent studies linked HSV-1 to neurodegenerative processes related to age-related disorders such as Alzheimer’s disease. Here, we explored whether recurrent HSV-1 infection might [...] Read more.
Herpes simplex virus 1 (HSV-1) is a widespread neurotropic virus establishing a life-long latent infection in neurons with periodic reactivations. Recent studies linked HSV-1 to neurodegenerative processes related to age-related disorders such as Alzheimer’s disease. Here, we explored whether recurrent HSV-1 infection might accelerate aging in neurons, focusing on peculiar marks of aged cells, such as the increase in histone H4 lysine (K) 16 acetylation (ac) (H4K16ac); the decrease of H3K56ac, and the modified expression of Sin3/HDAC1 and HIRA proteins. By exploiting both in vitro and in vivo models of recurrent HSV-1 infection, we found a significant increase in H4K16ac, Sin3, and HDAC1 levels, suggesting that the neuronal response to virus latency and reactivation includes the upregulation of these aging markers. On the contrary, we found a significant decrease in H3K56ac that was specifically linked to viral reactivation and apparently not related to aging-related markers. A complex modulation of HIRA expression and localization was found in the brain from HSV-1 infected mice suggesting a specific role of this protein in viral latency and reactivation. Overall, our results pointed out novel molecular mechanisms through which recurrent HSV-1 infection may affect neuronal aging, likely contributing to neurodegeneration. Full article
(This article belongs to the Special Issue Changes Produced by Viruses and Bacteria on the Nervous System)
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18 pages, 7720 KiB  
Article
Human Herpesvirus-6 and -7 in the Brain Microenvironment of Persons with Neurological Pathology and Healthy People
by Sandra Skuja, Simons Svirskis and Modra Murovska
Int. J. Mol. Sci. 2021, 22(5), 2364; https://doi.org/10.3390/ijms22052364 - 27 Feb 2021
Cited by 11 | Viewed by 2481
Abstract
During persistent human beta-herpesvirus (HHV) infection, clinical manifestations may not appear. However, the lifelong influence of HHV is often associated with pathological changes in the central nervous system. Herein, we evaluated possible associations between immunoexpression of HHV-6, -7, and cellular immune response across [...] Read more.
During persistent human beta-herpesvirus (HHV) infection, clinical manifestations may not appear. However, the lifelong influence of HHV is often associated with pathological changes in the central nervous system. Herein, we evaluated possible associations between immunoexpression of HHV-6, -7, and cellular immune response across different brain regions. The study aimed to explore HHV-6, -7 infection within the cortical lobes in cases of unspecified encephalopathy (UEP) and nonpathological conditions. We confirmed the presence of viral DNA by nPCR and viral antigens by immunohistochemistry. Overall, we have shown a significant increase (p < 0.001) of HHV antigen expression, especially HHV-7 in the temporal gray matter. Although HHV-infected neurons were found notably in the case of HHV-7, our observations suggest that higher (p < 0.001) cell tropism is associated with glial and endothelial cells in both UEP group and controls. HHV-6, predominantly detected in oligodendrocytes (p < 0.001), and HHV-7, predominantly detected in both astrocytes and oligodendrocytes (p < 0.001), exhibit varying effects on neural homeostasis. This indicates a high number (p < 0.001) of activated microglia observed in the temporal lobe in the UEP group. The question remains of whether human HHV contributes to neurological diseases or are markers for some aspect of the disease process. Full article
(This article belongs to the Special Issue Changes Produced by Viruses and Bacteria on the Nervous System)
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Review

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17 pages, 2795 KiB  
Review
Functions of Astrocytes under Normal Conditions and after a Brain Disease
by Soraya L. Valles, Sandeep Kumar Singh, Juan Campos-Campos, Carlos Colmena, Ignacio Campo-Palacio, Kenia Alvarez-Gamez, Oscar Caballero and Adrian Jorda
Int. J. Mol. Sci. 2023, 24(9), 8434; https://doi.org/10.3390/ijms24098434 - 8 May 2023
Cited by 9 | Viewed by 6834
Abstract
In the central nervous system (CNS) there are a greater number of glial cells than neurons (between five and ten times more). Furthermore, they have a greater number of functions (more than eight functions). Glia comprises different types of cells, those of neural [...] Read more.
In the central nervous system (CNS) there are a greater number of glial cells than neurons (between five and ten times more). Furthermore, they have a greater number of functions (more than eight functions). Glia comprises different types of cells, those of neural origin (astrocytes, radial glia, and oligodendroglia) and differentiated blood monocytes (microglia). During ontogeny, neurons develop earlier (at fetal day 15 in the rat) and astrocytes develop later (at fetal day 21 in the rat), which could indicate their important and crucial role in the CNS. Analysis of the phylogeny reveals that reptiles have a lower number of astrocytes compared to neurons and in humans this is reversed, as there have a greater number of astrocytes compared to neurons. These data perhaps imply that astrocytes are important and special cells, involved in many vital functions, including memory, and learning processes. In addition, astrocytes are involved in different mechanisms that protect the CNS through the production of antioxidant and anti-inflammatory proteins and they clean the extracellular environment and help neurons to communicate correctly with each other. The production of inflammatory mediators is important to prevent changes in brain homeostasis. On the contrary, excessive, or continued production appears as a characteristic element in many diseases, such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and in neurodevelopmental diseases, such as bipolar disorder, schizophrenia, and autism. Furthermore, different drugs and techniques have been developed to reverse oxidative stress and/or excess of inflammation that occurs in many CNS diseases, but much remains to be investigated. This review attempts to highlight the functional relevance of astrocytes in normal and neuropathological conditions by showing the molecular and cellular mechanisms of their role in the CNS. Full article
(This article belongs to the Special Issue Changes Produced by Viruses and Bacteria on the Nervous System)
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18 pages, 1635 KiB  
Review
The Nerves to Conduct a Multiple Sclerosis Crime Investigation
by Sameeksha Chopra, Zoë Myers, Henna Sekhon and Antoine Dufour
Int. J. Mol. Sci. 2021, 22(5), 2498; https://doi.org/10.3390/ijms22052498 - 2 Mar 2021
Cited by 2 | Viewed by 3466
Abstract
Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative autoimmune disease characterized by the aberrant infiltration of immune cells into the central nervous system (CNS) and by the loss of myelin. Sclerotic lesions and various inhibitory factors hamper the remyelination processes within the CNS. [...] Read more.
Multiple sclerosis (MS) is a chronic inflammatory neurodegenerative autoimmune disease characterized by the aberrant infiltration of immune cells into the central nervous system (CNS) and by the loss of myelin. Sclerotic lesions and various inhibitory factors hamper the remyelination processes within the CNS. MS patients typically experience gradual cognitive and physical disabilities as the disease progresses. The etiology of MS is still unclear and emerging evidence suggests that microbiome composition could play a much more significant role in disease pathogenesis than was initially thought. Initially believed to be isolated to the gut microenvironment, we now know that the microbiome plays a much broader role in various tissues and is essential in the development of the immune system. Here, we present some of the unexpected roles that the microbiome plays in MS and discuss approaches for the development of next-generation treatment strategies. Full article
(This article belongs to the Special Issue Changes Produced by Viruses and Bacteria on the Nervous System)
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