scholarly journals Review of the pathogenesis, clinical manifestations and peculiarities of neuropsychic disorders caused by COVID-19

2021 ◽  
Keyword(s):  
Nervous System ◽  
Human Body ◽  
Viral Entry ◽  
Clinical Manifestations ◽  
Circumventricular Organs ◽  
Brain Parenchyma ◽  
Human Cells ◽  
Host Cells ◽  
Monocyte Chemoattractant Protein 1 ◽  
Available Information

The article presents literature data numerous studies of patients with COVID-19. The available information helps to explain the nature and structure of the virus, the ways of penetration and its distribution in the human body, its interaction with the immune, nervous, endocrine, vascular, muscular systems, as well as the pathogenesis, clinic, diagnosis and treatment of this contingent of patients. Due to tropisms SARS-CoV-2 to the human cells specifi c S glycoprotein this virus can bind receptor human angiotensin-converting enzyme 2 (ACE-2), fuse with host cells and disseminate in the organism. Renin-angiotensin-aldosteron system (RAAS) plays an important role in regulation of blood vessels, heart, kidneys functions. ACE-2 has an infl uence on the infl ammatory, fi brotic and immunomodulatory mechanisms. Inhibition of these protection functions due to spread SARS-CoV-2 in human body leads to the progression of cardiovascular, renal and pulmonary diseases. Some authors describe indirectly the viral entry into the brain parenchyma by infecting the T-lymphocytes, that usually is accompanied by infl ammatory reactions with an increase in the specifi c cytokines such as interleukins (IL) — 6, IL-8, tumor necrosis factor, monocyte chemoattractant protein-1 (MCP-1). The peculiarities of the binding of the virus to the human cells are the presence of neurotropic properties and the ability to change the permeability of blood brain barier (BBB). Other authors note that the virus crosses the BBB directly through the olfactory neurons and also the brain’s circumventricular organs structures, surrounding the third and fourth ventricles, and promote the infection of nervous system. It can also cause intravascular coagulation and blood clotting, which may lead to various diseases of the nervous system. In this regard, an important task for neurologists is to further study the eff ect of the COVID-19 virus on the nervous system and prevent the occurrence of its complications.

scholarly journals SARS-CoV-2 Impact on the Central Nervous System: Are Astrocytes and Microglia Main Players or Merely Bystanders?

2020 ◽  
Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto Javier Ramos
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Experimental Models ◽  
Circumventricular Organs ◽  
Target Cells ◽  
Neurological Manifestations ◽  
Cns Inflammation ◽  
The Central Nervous System

With confirmed COVID-19 cases surpassing the 8.5 million mark around the globe, there is an imperative need to deepen the efforts from the international scientific community to gain comprehensive understanding of SARS-CoV-2. Although the main clinical manifestations are associated with respiratory or intestinal symptoms, reports of specific and non-specific neurological signs and symptoms, both at presentation or during the course of the acute phase, are increasing. Approximately 25-40% of the patients present neurological symptoms. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the Central Nervous System (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier (BBB). Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for MERS-CoV. Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to dysbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this work we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV, explore the potential role for astrocytes and microglia in the infection and neuroinflammation, and compare them with the previously described human and animal CoV that showed neurotropism. We also propose possible underlying mechanisms by focusing on our knowledge of glia, neurons, and their dynamic intricate communication with the immune system.

scholarly journals Histopathological features of SARS-CoV-2 infection and relationships with organoid technology

2021 ◽  
Vol 49 (9) ◽  
pp. 030006052110443
Author(s):  
İrem İnanç ◽  
Esra Erdemli
Keyword(s):  
Viral Entry ◽  
Three Dimensional ◽  
Human Cells ◽  
Host Cells ◽  
Angiotensin Converting Enzyme 2 ◽  
Antiviral Compounds ◽  
Global Pandemic ◽  
Species Specific

Coronavirus disease 2019 (COVID-19) following infection by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused a global pandemic that is still having serious effects worldwide. This virus, which targets the lungs in particular, can also damage other tissues. Angiotensin converting enzyme 2 (ACE-2) plays a key role in viral entry into host cells. The presence of ACE-2 in various tissues may permit viral infection. Studies of COVID-19 often make use of postmortem tissues. Although this information provides various useful results, it is also necessary to conduct in vitro studies to understand optimal treatment approaches. Because the virus may show species-specific differences, in vitro technologies using human cells are particularly important. Organoid technologies, three-dimensional structures that can be obtained from human cells, are playing increasingly important roles in studies of SARS-CoV-2. This technology offers a significant advantage in terms of mimicking in vivo tissue structures and testing antiviral compounds. In this mini-review, we summarize studies of SARS-CoV-2 using both histopathological and organoid technology approaches.

scholarly journals Variable Clinical Manifestations of COVID-19; Viral and Human Genomes Talk

2020 ◽  
Author(s):  
Zeinab Imani-Saber ◽  
Hajar Vaseghi ◽  
Mojdeh Mahdian ◽  
Fatemeh Safari ◽  
Mohsen Ghadami
Keyword(s):  
Viral Entry ◽  
Drug Transport ◽  
Phylogenetic Analyses ◽  
Clinical Manifestations ◽  
Host Cells ◽  
World Health ◽  
Ongoing Research ◽  
Transmission Mechanisms ◽  
Human Genomes ◽  
Health Organization

The new coronavirus, known as “SARS-CoV-2”; is the cause of one of the most prevalent infectious viral diseases that was recently announced pandemic by the world health organization. Ongoing research in the fields of prevention, management, and therapy establishes a functional scaffold for clinics during the time of crisis. To obtain this goal, it is necessary that all pathophysiologic aspects of COVID-19 from infection to predisposing backgrounds of infection be identified, so that all the ambiguities of researchers regarding transmission mechanisms, variable clinical manifestation, and therapeutic response can be solved. Here, we firstly discuss about the homology screening between nCoV-2019 and beta-coronavirus family using phylogenetic analyses. Secondly, we analyzed the viral motifs to show that viral entry into the host cells requires a primary activation step performed by FURIN and FURIN-like-mediated enzymatic cleavage on the structural glycoprotein. The cleavage increases viral performance by 1000 folds. We then present a comprehensive view on host cells and the significance of gene variants affecting activation enzymes, supportive entry, and spread mechanisms in humans including renin-angiotensin-aldosterone system (RAAS) a pathway results in certain phenotypes or exacerbate infection-related phenotypes in different organs, hence causes variable clinical manifestations. This is followed by discussing about the importance of personalized medicine in nCoV-2019 exposure. Moreover, chemical drugs prescribed for individuals affected with COVID-19, as well as genes involved in drug transport and metabolisms are reviewed as a prelude to drug response. Finally, we suggest some therapeutic approaches developed based on new methods and technology such as anti-sense therapy and antibodies.

scholarly journals Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry by Neisseria meningitidis across the Blood–Brain Barriers

2020 ◽  
Vol 21 (22) ◽  
pp. 8788
Author(s):  
Julia Borkowski ◽  
Horst Schroten ◽  
Christian Schwerk
Keyword(s):  
Signal Transduction ◽  
Central Nervous System ◽  
Nervous System ◽  
Neisseria Meningitidis ◽  
Severe Disease ◽  
Blood Stream ◽  
Brain Parenchyma ◽  
Host Cells ◽  
Signal Transduction Pathways ◽  
Blood Brain

The Gram-negative diplococcus Neisseria meningitidis, also called meningococcus, exclusively infects humans and can cause meningitis, a severe disease that can lead to the death of the afflicted individuals. To cause meningitis, the bacteria have to enter the central nervous system (CNS) by crossing one of the barriers protecting the CNS from entry by pathogens. These barriers are represented by the blood–brain barrier separating the blood from the brain parenchyma and the blood–cerebrospinal fluid (CSF) barriers at the choroid plexus and the meninges. During the course of meningococcal disease resulting in meningitis, the bacteria undergo several interactions with host cells, including the pharyngeal epithelium and the cells constituting the barriers between the blood and the CSF. These interactions are required to initiate signal transduction pathways that are involved during the crossing of the meningococci into the blood stream and CNS entry, as well as in the host cell response to infection. In this review we summarize the interactions and pathways involved in these processes, whose understanding could help to better understand the pathogenesis of meningococcal meningitis.

scholarly journals Severe Acute Respiratory Syndrome Coronavirus 2 Impact on the Central Nervous System: Are Astrocytes and Microglia Main Players or Merely Bystanders?

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142095496 ◽  
Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto J. Ramos
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Severe Acute Respiratory Syndrome ◽  
Clinical Manifestations ◽  
Experimental Models ◽  
Circumventricular Organs ◽  
Target Cells ◽  
Neurological Manifestations ◽  
Cns Inflammation ◽  
The Central Nervous System

With confirmed coronavirus disease 2019 (COVID-19) cases surpassing the 18 million mark around the globe, there is an imperative need to gain comprehensive understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the main clinical manifestations of COVID-19 are associated with respiratory or intestinal symptoms, reports of neurological signs and symptoms are increasing. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the central nervous system (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood–brain barrier. Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS rennin-angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for Middle East respiratory syndrome coronavirus (MERS-CoV). Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes, and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to disbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this comprehensive review, we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV; explore the potential role for astrocytes and microglia in the infection and neuroinflammation; and compare them with the previously described human and animal CoV that showed neurotropism to propose possible underlying mechanisms.

scholarly journals Lack of Functional Receptors Is the Only Barrier That Prevents Caprine Arthritis-Encephalitis Virus from Infecting Human Cells

2000 ◽  
Vol 74 (18) ◽  
pp. 8343-8348 ◽  
Author(s):  
Laila Mselli-Lakhal ◽  
Colette Favier ◽  
Kevin Leung ◽  
Francois Guiguen ◽  
Delphine Grezel ◽  
...  
Keyword(s):  
Host Cell ◽  
Viral Entry ◽  
Human Cells ◽  
Encephalitis Virus ◽  
Host Cells ◽  
Productive Infection ◽  
Caprine Arthritis Encephalitis Virus ◽  
Successful Infection ◽  
Host Cell Surface ◽  
Vesicular Stomatitis

ABSTRACT Barriers to replication of viruses in potential host cells may occur at several levels. Lack of suitable and functional receptors on the host cell surface, thereby precluding entry of the virus, is a frequent reason for noninfectivity, as long as no alternative way of entry (e.g., pinocytosis, antibody-dependent adsorption) can be exploited by the virus. Other barriers can intervene at later stages of the virus life cycle, with restrictions on transcription of the viral genome, incorrect translation and posttranslational processing of viral proteins, inefficient viral assembly, and release or efficient early induction of apoptosis in the infected cell. The data we present here demonstrate that replication of caprine arthritis-encephalitis virus (CAEV) is restricted in a variety of human cell lines and primary tissue cultures. This barrier was efficiently overcome by transfection of a novel infectious complete-proviral CAEV construct into the same cells. The successful infection of human cells with a vesicular stomatitis virus (VSV) G-pseudotyped Env-defective CAEV confirmed that viral entry is the major obstacle to CAEV infection of human cells. The fully efficient productive infection obtained with the VSV-G-protein-pseudotyped infectious CAEV strengthened the evidence that lack of viral entry is the only practical barrier to CAEV replication in human cells. The virus thus produced retained its original host cell specificity and acquired no propensity to propagate further in human cultures.

scholarly journals Neurological disorders of COVID-19 can be explained in terms of “loss or gain of function” of a solution for the nervous system

2021 ◽  
Author(s):  
Kunjumon Ittira Vadakkan
Keyword(s):  
Nervous System ◽  
Viral Entry ◽  
Neurological Disorders ◽  
Close Contact ◽  
Host Cells ◽  
Gain Of Function ◽  
Host Cell Membrane ◽  
Adaptation Mechanism ◽  
Vesicle Exocytosis ◽  
Cellular Fusion

Background: Covid-19 infection causes several neurological disorders. Even though it is still not known how the brain works, there are models of its operational mechanism. Semblance hypothesis has derived a mechanism of nervous system functions whose keystone structural change is inter-postsynaptic LINK (IPL) formed by a spectrum of interactions between spines that belong to different neurons. These interactions range from close contact between membranes of spines to partial and complete hemifusion between them.Recent developments: Covid-19 spike protein is a fusion protein that in addition to generating fusion pores in the host cell membrane for viral entry, also forms inter-cellular fusion between host cells. When virus exits a cell by vesicle exocytosis, it can cause fusion of the hemifused area of IPL, which is a bilayer structure,. An adaptation mechanism that prevents progression of hemifusion to fusion is expected to deteriorate during aging and may prevent reversal of IPL fusion. Since analyses have shown that transcriptomes of even adjacent neurons of same type are different in the cortex, inter-cellular fusion can lead to protein precipitation within spines that can lead to spine loss and eventual neuronal death. Furthermore, formation of non-specific IPLs can lead to “gain of function” changes responsible for some of the neurological features of COVID-19. Where next? Since neurological symptoms of COVID-19 can be explained in terms of “loss or gain of function” of the derived structure-function mechanism of IPL, it motivates undertaking verification of IPLs. Expected size of an IPL is nearly ten square nanometers. It is necessary to conduct dedicated studies using advanced microscopic methods to verify formation of IPLs and invent methods to study units of inner sensations at the inter-LINKed spines and their computations.

scholarly journals EXTENSIVELY DISSEMINATED CYSTICERCOSIS – CASE REPORT AND REVIEW OF LITERATURE

2020 ◽  
pp. 68-69
Author(s):  
Navdeep Kaur ◽  
Narinder Kaur ◽  
Harvinder Singh Chhabra ◽  
Ravinder Kaur
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Case Report ◽  
Clinical Manifestations ◽  
Brain Parenchyma ◽  
Review Of Literature ◽  
Rare Presentation ◽  
Subcutaneous Nodules ◽  
The Central Nervous System ◽  
High Index Of Suspicion

Cysticercosis is a known disease of the developing world and accounts for the majority of epilepsy cases in these nations. The disseminated form represents a rare presentation of the disease with neurocysticercosis being the most common. Patients may present with neurological complaints of seizures only with no clinical manifestations of muscular pseudohypertrophy or palpable subcutaneous nodules usually found in disseminated form falsely localizing disease to the central nervous system. This case report highlights the fact that despite its rarity a high index of suspicion for disseminated form should be kept in mind in endemic areas and warrants routine screening of all patients for multi-organ involvement who present with multiple lesions in brain parenchyma.

DIAGNOSTIC VALUE OF SPECIFIC ANTIBODY SYNTHESIS IN BRAIN OF PATIENTS WITH NEUROINFECTIONS

2019 ◽  
Vol 72 (8) ◽  
pp. 1437-1441
Author(s):  
Pavel Dyachenko ◽  
Igor Filchakov ◽  
Anatoly Dyachenko ◽  
Victoria Kurhanskaya
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Manifestations ◽  
Diagnostic Value ◽  
Diagnostic Challenge ◽  
Specific Antibodies ◽  
Intrathecal Synthesis ◽  
Varicella Zoster ◽  
Mrz Reaction ◽  
Wide Range

Introduction: Viral encephalitis accounts for 40-70% of all cases worldwide, central nervous system infections pose a diagnostic challenge because clinical manifestations are not typically pathognomonic for specific pathogens, and a wide range of agents can be causative. The aim: To assess the diagnostic value of intrathecal synthesis of specific antibodies in patients with inflammatory lesions of the central nervous system. Materials and methods: Within the framework of the study, two groups of 90 people in each were formed from the patients with neuroinfections admitted to our Center. Intrathecal synthesis (ITS) of total (unspecific) IgG in members of one of group (group of compare) was determined. Brain synthesis of specific antibodies (Ab) to some neurotropic pathogens (herpes simplex virus 1/2, cytomegalovirus, Epstein-Barr virus, varicella zoster virus, rubella virus, Borrelies) was studied in the second group of patients (group of interest). There were no statistically significant differences between groups by gender and age. Encephalitis and encephalomyelitis prevailed among patients of both groups Results: ITS of total IgG was established in 30 (33.3 ± 6.1 %) patients of the first group with IgG index more than 0.6 indicating on inflammatory process in CNS and no marked changes of CSF. ITS of specific Ab was determined in 23 of 90 (25.6 ± 4.6 %) patients included into group of interest. In more than half of cases Ab to several infectious agents were detected simultaneously. ITS of various specificity, in particular, to measles and rubella viruses, and VZV, known as MRZ-reaction, is characteristic of some autoimmune lesions of CNS, multiple sclerosis first of all. In fact, further research of 5 patients with MRZ-reaction confirmed their autoimmune failure of CNS. Detection of ITS in the CSF samples didn’t depend on concentration of specific Ab in serum and CSF and wasn’t followed by HEB dysfunctions which were observed with the same frequency in patients with or without ITS (13.0 % and 13.6 % respectively). Conclusion: Specific Ab synthesis to several neurotropic pathogens in the CSF of significant part of examined patients was established. Thus, diagnostic value of ITS of specific immunoglobulins seems to be limited to cases in which autoimmune damage of the CNS is suspected.

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