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2.
Front Immunol ; 12: 752557, 2021.
Article in English | MEDLINE | ID: covidwho-1789371

ABSTRACT

Objective: To analyze and compare different clinical, laboratory, and magnetic resonance imaging characteristics between pediatric and adult patients with first-attack myelin oligodendrocyte glycoprotein antibody disease (MOGAD) and to explore predictive factors for severity at disease onset. Methods: Patients diagnosed with MOGAD at the First Affiliated Hospital of Zhengzhou University from January 2013 to August 2021 were enrolled in this retrospective study. Age at disease onset, sex, comorbidities, laboratory tests, magnetic resonance imaging (MRI) characteristics, and Expanded Disability Status Scale (EDSS) scores were collected and analyzed. The association between risk factors and initial EDSS scores at disease onset was analyzed using logistic regression models and Spearman correlation analyses. A receiver-operating characteristic (ROC) curve analysis was used to evaluate the predictive ability of the uric acid and homocysteine (Hcy) levels for the severity of neurological dysfunction at the onset of MOGAD. Results: Sixty-seven patients (female, n=34; male, n=33) with first-attack MOGAD were included in this study. The mean age at onset was 26.43 ± 18.22 years (range: 3-79 years). Among patients <18 years of age, the most common presenting symptoms were loss of vision (36.0%), and nausea and vomiting (24.0%), and the most common disease spectrum was acute disseminated encephalomyelitis (ADEM) (40.0%). Among patients aged ≥18 years, the most common presenting symptoms were loss of vision (35.7%), paresthesia (33.3%), and paralysis (26.2%), and the most common disease spectrum was optic neuritis (35.7%). The most common lesions were cortical gray matter/paracortical white matter lesions in both pediatric and adult patients. Uric acid [odds ratio (OR)=1.014; 95% confidence interval (CI)=1.006-1.022; P=0.000] and serum Hcy (OR=1.125; 95% CI=1.017-1.246; P=0.023) levels were significantly associated with the severity of neurological dysfunction at disease onset. Uric acid levels (r=0.2583; P=0.035) and Hcy levels (r=0.3971; P=0.0009) were positively correlated with initial EDSS scores. The areas under the ROC curve were 0.7775 (95% CI= 0.6617‒0.8933; P<0.001) and 0.6767 (95% CI=0.5433‒0.8102, P=0.014) for uric acid and Hcy levels, respectively. Conclusion: The clinical phenotype of MOGAD varies in patients of different ages. The most common disease spectrum was ADEM in patients aged<18 years, while optic neuritis was commonly found in patients aged ≥18 years. The uric acid and Hcy levels are risk factors for the severity of neurological dysfunction at disease onset in patients with first-attack MOGAD.


Subject(s)
Autoantibodies/immunology , Autoimmune Diseases of the Nervous System/epidemiology , Myelin-Oligodendrocyte Glycoprotein/immunology , Adolescent , Adult , Age of Onset , Aged , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/diagnosis , Autoimmune Diseases of the Nervous System/diagnostic imaging , Autoimmune Diseases of the Nervous System/immunology , Autoimmune Diseases of the Nervous System/metabolism , Biomarkers , Central Nervous System/diagnostic imaging , Cerebrospinal Fluid Proteins/analysis , Child , Child, Preschool , China/epidemiology , Comorbidity , Diagnosis, Differential , Female , Follow-Up Studies , Homocysteine/blood , Humans , Immunosuppressive Agents/therapeutic use , Magnetic Resonance Imaging , Male , Middle Aged , Risk Factors , Severity of Illness Index , Single-Blind Method , Uric Acid/blood , Young Adult
3.
Curr Neuropharmacol ; 20(4): 777-781, 2022.
Article in English | MEDLINE | ID: covidwho-1785246

ABSTRACT

BACKGROUND: As the World faces unprecedented pandemic caused by SARS-CoV-2 virus, repositioning of existing drugs to treatment of COVID-19 disease is urgently awaited, provided that high quality scientific evidence supporting safety and efficacy in this new indication is gathered. Efforts concerning drugs repositioning to COVID-19 were mostly focused on antiviral drugs, or drugs targeting the late phase of the disease. METHODS: Based on published research, the pharmacological activities of fluvoxamine and amantadine, two well-known drugs widely used in clinical practice for psychiatric and neurological diseases, respectively, have been reviewed, with a focus on their potential therapeutic importance in the treatment of COVID-19. RESULTS: Several preclinical and clinical reports were identified suggesting that these two drugs might exert protective effects in the early phases of COVID-19. CONCLUSION: Preclinical and early clinical evidence are presented indicating that these drugs hold promise to prevent COVID-19 progression when administered early during the course of infection.


Subject(s)
COVID-19 , Fluvoxamine , Amantadine/therapeutic use , Antiviral Agents/therapeutic use , COVID-19/drug therapy , Central Nervous System , Central Nervous System Agents , Fluvoxamine/therapeutic use , Humans , SARS-CoV-2
4.
Front Public Health ; 9: 738412, 2021.
Article in English | MEDLINE | ID: covidwho-1775888

ABSTRACT

Background: Unbiased metagenomic next-generation sequencing (mNGS) detects pathogens in a target-independent manner. It is not well-understood whether mNGS has comparable sensitivity to target-dependent nucleic acid test for pathogen identification. Methods: This study included 31 patients with chickenpox and neurological symptoms for screening of possible varicella-zoster virus (VZV) central nervous system (CNS) infection. Microbiological diagnosing of VZV cerebrospinal fluid (CSF) infection was performed on stored CSF samples using mNGS, quantitative and qualitative VZV-specific PCR assays, and VZV IgM antibodies test. Results: The median age was 30.0 [interquartile range (IQR), 24.3-33.3] years. 51.6% of the patients were men. About 80.6% of the patients had normal CSF white blood cell counts (≤ 5 × 106/L). VZV IgM antibodies presented in 16.1% of the CSF samples, and nucleic acids were detectable in 16.1 and 9.7% using two different VZV-specific real-time PCR protocols. Intriguingly, maximal identification of VZV elements was achieved by CSF mNGS (p = 0.001 and p = 007; compared with qualitative PCR and VZV IgM antibody test, respectively), with sequence reads of VZV being reported in 51.6% (16/31) of the CSF samples. All VZV PCR positive samples were positive when analyzed by mNGS. Of note, human betaherpesvirus 6A with clinical significance was unexpectedly detected in one CSF sample. Conclusions: Our study suggests that CSF mNGS may have higher sensitivity for VZV detection than CSF VZV PCR and antibody tests, and has the advantage of identifying unexpected pathogens.


Subject(s)
Central Nervous System Infections , Chickenpox , Adult , Central Nervous System , Herpesvirus 3, Human/genetics , High-Throughput Nucleotide Sequencing/methods , Humans , Male
5.
Front Immunol ; 13: 833548, 2022.
Article in English | MEDLINE | ID: covidwho-1771039

ABSTRACT

The direct impact and sequelae of infections in children and adults result in significant morbidity and mortality especially when they involve the central (CNS) or peripheral nervous system (PNS). The historical understanding of the pathophysiology has been mostly focused on the direct impact of the various pathogens through neural tissue invasion. However, with the better understanding of neuroimmunology, there is a rapidly growing realization of the contribution of the innate and adaptive host immune responses in the pathogenesis of many CNS and PNS diseases. The balance between the protective and pathologic sequelae of immunity is fragile and can easily be tipped towards harm for the host. The matter of immune privilege and surveillance of the CNS/PNS compartments and the role of the blood-brain barrier (BBB) and blood nerve barrier (BNB) makes this even more complex. Our understanding of the pathogenesis of many post-infectious manifestations of various microbial agents remains elusive, especially in the diverse African setting. Our exploration and better understanding of the neuroimmunology of some of the infectious diseases that we encounter in the continent will go a long way into helping us to improve their management and therefore lessen the burden. Africa is diverse and uniquely poised because of the mix of the classic, well described, autoimmune disease entities and the specifically "tropical" conditions. This review explores the current understanding of some of the para- and post-infectious autoimmune manifestations of CNS and PNS diseases in the African context. We highlight the clinical presentations, diagnosis and treatment of these neurological disorders and underscore the knowledge gaps and perspectives for future research using disease models of conditions that we see in the continent, some of which are not uniquely African and, where relevant, include discussion of the proposed mechanisms underlying pathogen-induced autoimmunity. This review covers the following conditions as models and highlight those in which a relationship with COVID-19 infection has been reported: a) Acute Necrotizing Encephalopathy; b) Measles-associated encephalopathies; c) Human Immunodeficiency Virus (HIV) neuroimmune disorders, and particularly the difficulties associated with classical post-infectious autoimmune disorders such as the Guillain-Barré syndrome in the context of HIV and other infections. Finally, we describe NMDA-R encephalitis, which can be post-HSV encephalitis, summarise other antibody-mediated CNS diseases and describe myasthenia gravis as the classic antibody-mediated disease but with special features in Africa.


Subject(s)
Brain Diseases , COVID-19 , Central Nervous System Diseases , Communicable Diseases , Encephalitis , Peripheral Nervous System Diseases , Adult , Autoimmunity , Central Nervous System , Child , Humans , Peripheral Nervous System
6.
J Neuroimaging ; 32(1): 104-110, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1769736

ABSTRACT

BACKGROUND AND PURPOSE: Treatment of elevated intracranial pressure (ICP) is central to neurocritical care, but not all patients are eligible for invasive ICP-monitoring. A promising noninvasive option is ultrasound measurement of the optic nerve sheath diameter (ONSD). However, meta-analyses of ONSD for elevated ICP show wide confidence intervals. This might be due to baseline variations, inter-rater variability, and varying measurement methods. No standardized protocol has been validated. Corrections for eyeball diameter (ED) and optic nerve diameter (OND) may compensate for baseline variations. We evaluated a protocol and compared two different measurement methods for ONSD ultrasound. METHODS: Two operators, blinded to each other's measurements, measured ONSD, ED, and OND twice in 20 patients. ONSD was measured with two different methods in use: internal (ONSDint) or external (ONSDext) of the dura mater. Intra-class correlation (ICC) was calculated for inter-rater and intra-rater reliability. RESULTS: ICCs for inter-rater reliability of ONSDext and ONSDint (95% confidence interval) were 0.96 (0.93, 0.98) and 0.88 (0.79, 0.94), respectively. ICCs for intra-rater reliability of ONSDext and ONSDint were 0.97 (0.94, 0.99) and 0.93 (0.87, 0.96), respectively. There was no significant bias or difference in intra-rater reliability between operators. CONCLUSIONS: ONSD can be measured with an excellent inter- and intra-rater reliability and low risk of inter-rater bias, when using this protocol. ONSDext yields a higher inter- and intra-rater reliability than ONSDint. Corrections for ED and OND can be performed reliably.


Subject(s)
Intracranial Hypertension , Central Nervous System , Humans , Intracranial Hypertension/diagnostic imaging , Intracranial Pressure/physiology , Optic Nerve/diagnostic imaging , Reproducibility of Results , Ultrasonography/methods
7.
Cell Mol Biol Lett ; 27(1): 10, 2022 Feb 02.
Article in English | MEDLINE | ID: covidwho-1753103

ABSTRACT

The novel coronavirus disease 2019 (COVID-19) pandemic has spread worldwide, and finding a safe therapeutic strategy and effective vaccine is critical to overcoming severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Therefore, elucidation of pathogenesis mechanisms, especially entry routes of SARS-CoV-2 may help propose antiviral drugs and novel vaccines. Several receptors have been demonstrated for the interaction of spike (S) protein of SARS-CoV-2 with host cells, including angiotensin-converting enzyme (ACE2), ephrin ligands and Eph receptors, neuropilin 1 (NRP-1), P2X7, and CD147. The expression of these entry receptors in the central nervous system (CNS) may make the CNS prone to SARS-CoV-2 invasion, leading to neurodegenerative diseases. The present review provides potential pathological mechanisms of SARS-CoV-2 infection in the CNS, including entry receptors and cytokines involved in neuroinflammatory conditions. Moreover, it explains several neurodegenerative disorders associated with COVID-19. Finally, we suggest inflammasome and JaK inhibitors as potential therapeutic strategies for neurodegenerative diseases.


Subject(s)
COVID-19/drug therapy , Central Nervous System/drug effects , Inflammasomes/drug effects , Neurodegenerative Diseases/drug therapy , Receptors, Virus/genetics , SARS-CoV-2/drug effects , Virus Internalization/drug effects , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/metabolism , Antiviral Agents/therapeutic use , Basigin/genetics , Basigin/metabolism , COVID-19/genetics , COVID-19/metabolism , COVID-19/virology , Central Nervous System/metabolism , Central Nervous System/virology , Ephrins/genetics , Ephrins/metabolism , Gene Expression Regulation , Host-Pathogen Interactions/drug effects , Host-Pathogen Interactions/genetics , Humans , Immunologic Factors/therapeutic use , Inflammasomes/genetics , Inflammasomes/metabolism , Janus Kinase Inhibitors/therapeutic use , Janus Kinases/antagonists & inhibitors , Janus Kinases/genetics , Janus Kinases/metabolism , Neurodegenerative Diseases/genetics , Neurodegenerative Diseases/metabolism , Neurodegenerative Diseases/virology , Neuropilin-1/genetics , Neuropilin-1/metabolism , Receptors, Purinergic P2X7/genetics , Receptors, Purinergic P2X7/metabolism , Receptors, Virus/antagonists & inhibitors , Receptors, Virus/metabolism , SARS-CoV-2/genetics , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Signal Transduction
8.
Fluids Barriers CNS ; 19(1): 19, 2022 Mar 01.
Article in English | MEDLINE | ID: covidwho-1717977

ABSTRACT

BACKGROUND: Scientific conferences are vital communication events for scientists in academia, industry, and government agencies. In the brain barriers research field, several international conferences exist that allow researchers to present data, share knowledge, and discuss novel ideas and concepts. These meetings are critical platforms for researchers to connect and exchange breakthrough findings on a regular basis. Due to the worldwide COVID-19 pandemic, all in-person meetings were canceled in 2020. In response, we launched the Brain Barriers Virtual 2020 (BBV2020) seminar series, the first stand-in virtual event for the brain barriers field, to offer scientists a virtual platform to present their work. Here we report the aggregate attendance information on two in-person meetings compared with BBV2020 and comment on the utility of the virtual platform. METHODS: The BBV2020 seminar series was hosted on a Zoom webinar platform and was free of cost for participants. Using registration- and Zoom-based data from the BBV2020 virtual seminar series and survey data collected from BBV2020 participants, we analyzed attendance trends, global reach, participation based on career stage, and engagement of BBV2020. We compared these data with those from two previous in-person conferences, a BBB meeting held in 2018 and CVB 2019. RESULTS: We found that BBV2020 seminar participation steadily decreased over the course of the series. In contrast, live participation was consistently above 100 attendees and recording views were above 200 views per seminar. We also found that participants valued BBV2020 as a supplement during the COVID-19 pandemic in 2020. Based on one post-BBV2020 survey, the majority of participants indicated that they would prefer in-person meetings but would welcome a virtual component to future in-person meetings. Compared to in-person meetings, BBV2020 enabled participation from a broad range of career stages and was attended by scientists in academic, industry, and government agencies from a wide range of countries worldwide. CONCLUSIONS: Our findings suggest that a virtual event such as the BBV2020 seminar series provides easy access to science for researchers across all career stages around the globe. However, we recognize that limitations exist. Regardless, such a virtual event could be a valuable tool for the brain barriers community to reach and engage scientists worldwide to further grow the brain barriers research field in the future.


Subject(s)
COVID-19 , Central Nervous System , Congresses as Topic , Videoconferencing , Humans , SARS-CoV-2 , Surveys and Questionnaires
9.
Stem Cell Reports ; 17(2): 307-320, 2022 02 08.
Article in English | MEDLINE | ID: covidwho-1712991

ABSTRACT

Neurological complications are common in COVID-19. Although SARS-CoV-2 has been detected in patients' brain tissues, its entry routes and resulting consequences are not well understood. Here, we show a pronounced upregulation of interferon signaling pathways of the neurovascular unit in fatal COVID-19. By investigating the susceptibility of human induced pluripotent stem cell (hiPSC)-derived brain capillary endothelial-like cells (BCECs) to SARS-CoV-2 infection, we found that BCECs were infected and recapitulated transcriptional changes detected in vivo. While BCECs were not compromised in their paracellular tightness, we found SARS-CoV-2 in the basolateral compartment in transwell assays after apical infection, suggesting active replication and transcellular transport of virus across the blood-brain barrier (BBB) in vitro. Moreover, entry of SARS-CoV-2 into BCECs could be reduced by anti-spike-, anti-angiotensin-converting enzyme 2 (ACE2)-, and anti-neuropilin-1 (NRP1)-specific antibodies or the transmembrane protease serine subtype 2 (TMPRSS2) inhibitor nafamostat. Together, our data provide strong support for SARS-CoV-2 brain entry across the BBB resulting in increased interferon signaling.


Subject(s)
Blood-Brain Barrier/virology , Central Nervous System/virology , SARS-CoV-2/physiology , Virus Internalization , Antibodies/pharmacology , Benzamidines/pharmacology , COVID-19/pathology , COVID-19/virology , Endothelial Cells/cytology , Endothelial Cells/metabolism , Endothelial Cells/virology , Guanidines/pharmacology , Humans , Induced Pluripotent Stem Cells/cytology , Induced Pluripotent Stem Cells/metabolism , Models, Biological , RNA, Viral/metabolism , Reverse Transcriptase Polymerase Chain Reaction , SARS-CoV-2/genetics , SARS-CoV-2/isolation & purification , Virus Internalization/drug effects
10.
J Virol ; 96(4): e0196921, 2022 02 23.
Article in English | MEDLINE | ID: covidwho-1702819

ABSTRACT

Unlike SARS-CoV-1 and MERS-CoV, infection with SARS-CoV-2, the viral pathogen responsible for COVID-19, is often associated with neurologic symptoms that range from mild to severe, yet increasing evidence argues the virus does not exhibit extensive neuroinvasive properties. We demonstrate SARS-CoV-2 can infect and replicate in human iPSC-derived neurons and that infection shows limited antiviral and inflammatory responses but increased activation of EIF2 signaling following infection as determined by RNA sequencing. Intranasal infection of K18 human ACE2 transgenic mice (K18-hACE2) with SARS-CoV-2 resulted in lung pathology associated with viral replication and immune cell infiltration. In addition, ∼50% of infected mice exhibited CNS infection characterized by wide-spread viral replication in neurons accompanied by increased expression of chemokine (Cxcl9, Cxcl10, Ccl2, Ccl5 and Ccl19) and cytokine (Ifn-λ and Tnf-α) transcripts associated with microgliosis and a neuroinflammatory response consisting primarily of monocytes/macrophages. Microglia depletion via administration of colony-stimulating factor 1 receptor inhibitor, PLX5622, in SARS-CoV-2 infected mice did not affect survival or viral replication but did result in dampened expression of proinflammatory cytokine/chemokine transcripts and a reduction in monocyte/macrophage infiltration. These results argue that microglia are dispensable in terms of controlling SARS-CoV-2 replication in in the K18-hACE2 model but do contribute to an inflammatory response through expression of pro-inflammatory genes. Collectively, these findings contribute to previous work demonstrating the ability of SARS-CoV-2 to infect neurons as well as emphasizing the potential use of the K18-hACE2 model to study immunological and neuropathological aspects related to SARS-CoV-2-induced neurologic disease. IMPORTANCE Understanding the immunological mechanisms contributing to both host defense and disease following viral infection of the CNS is of critical importance given the increasing number of viruses that are capable of infecting and replicating within the nervous system. With this in mind, the present study was undertaken to evaluate the role of microglia in aiding in host defense following experimental infection of the central nervous system (CNS) of K18-hACE2 with SARS-CoV-2, the causative agent of COVID-19. Neurologic symptoms that range in severity are common in COVID-19 patients and understanding immune responses that contribute to restricting neurologic disease can provide important insight into better understanding consequences associated with SARS-CoV-2 infection of the CNS.


Subject(s)
Angiotensin-Converting Enzyme 2/immunology , COVID-19/immunology , Central Nervous System Viral Diseases/immunology , Microglia/immunology , SARS-CoV-2/physiology , Virus Replication/immunology , Angiotensin-Converting Enzyme 2/genetics , Animals , COVID-19/genetics , Central Nervous System/immunology , Central Nervous System/virology , Central Nervous System Viral Diseases/genetics , Central Nervous System Viral Diseases/virology , Chemokines/genetics , Chemokines/immunology , Disease Models, Animal , Humans , Mice , Mice, Transgenic , Microglia/virology , Neurons/immunology , Neurons/virology , Virus Replication/genetics
11.
Arq Neuropsiquiatr ; 79(11): 1049-1061, 2021 11.
Article in English | MEDLINE | ID: covidwho-1674093

ABSTRACT

The Scientific Department of Neuroimmunology of the Brazilian Academy of Neurology (DCNI/ABN) and Brazilian Committee for Treatment and Research in Multiple Sclerosis and Neuroimmunological Diseases (BCTRIMS) provide recommendations in this document for vaccination of the population with demyelinating diseases of the central nervous system (CNS) against infections in general and against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes COVID-19. We emphasize the seriousness of the current situation in view of the spread of COVID-19 in our country. Therefore, reference guides on vaccination for clinicians, patients, and public health authorities are particularly important to prevent some infectious diseases. The DCNI/ABN and BCTRIMS recommend that patients with CNS demyelinating diseases (e.g., MS and NMOSD) be continually monitored for updates to their vaccination schedule, especially at the beginning or before a change in treatment with a disease modifying drug (DMD). It is also important to note that vaccines are safe, and physicians should encourage their use in all patients. Clearly, special care should be taken when live attenuated viruses are involved. Finally, it is important for physicians to verify which DMD the patient is receiving and when the last dose was taken, as each drug may affect the induction of immune response differently.


Subject(s)
COVID-19 , Multiple Sclerosis , Neurology , Central Nervous System , Humans , Multiple Sclerosis/drug therapy , SARS-CoV-2 , Vaccination
12.
Neurol Sci ; 43(4): 2171-2186, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1626343

ABSTRACT

The first case of coronavirus illness was discovered in Wuhan, China, in January 2020 and quickly spread worldwide within the next couple of months. The condition was initially only linked with respiratory disorders. After the evolution of various variants of the SARS-CoV-2, the critical impact of the virus spread to multiple organs and soon, neurological disorder manifestations started to appear in the infected patients. The review is focused on the manifestation of various neurological disorders linked with both the central nervous system and peripheral nervous system. Disorders such as cytokine release syndrome, encephalitis, acute stroke, and Bell's palsy are given specific attention and psychological manifestations are also investigated. For a clear conclusion, cognitive impairment, drug addiction disorders, mood and anxiety disorders, and post-traumatic stress disorder are all fully examined. The association of the SARS-CoV-2 with neurological disorders and pathway is yet to be clear. For better understanding, the explanation of the possible mechanism of viral infection influencing the nervous system is also attempted in the review. While several vaccines and drugs are already involved in treating the SARS-CoV-2 condition, the disease is still considered fatal and more likely to leave permanent neurological damage, which leads to an essential requirement for more research to explore the neurological toll of the COVID-19 disease.


Subject(s)
COVID-19 , Nervous System Diseases , Stroke , Central Nervous System , Humans , Nervous System Diseases/epidemiology , Nervous System Diseases/etiology , SARS-CoV-2
13.
J Pediatr Hematol Oncol ; 44(3): e723-e727, 2022 04 01.
Article in English | MEDLINE | ID: covidwho-1599071

ABSTRACT

B-cell acute lymphoblastic leukemia (B-ALL) is the most common pediatric malignancy with a highly favorable overall prognosis. Central nervous system (CNS) relapse of B-ALL is relatively rare and is associated with inferior survival outcomes. We present two patients with B-ALL who developed isolated CNS relapse following confirmed infection with severe acute respiratory syndrome coronavirus 2. In addition to individual and disease factors, we posit that delays in therapy together with immune system modulation because of severe acute respiratory syndrome coronavirus 2 may account for these 2 cases of CNS relapsed B-ALL. We report on this clinical observation to raise awareness of this potential association.


Subject(s)
COVID-19 , Central Nervous System Neoplasms , Precursor Cell Lymphoblastic Leukemia-Lymphoma , COVID-19/complications , Central Nervous System/pathology , Central Nervous System Neoplasms/therapy , Child , Humans , Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications , Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy , Recurrence , SARS-CoV-2
14.
Curr HIV/AIDS Rep ; 18(6): 538-548, 2021 12.
Article in English | MEDLINE | ID: covidwho-1540268

ABSTRACT

The convergence of the HIV and SARS-CoV-2 pandemics is an emerging field of interest. In this review, we outline the central nervous system (CNS) effects of COVID-19 in the general population and how these effects may manifest in people with HIV (PWH). We discuss the hypothetical mechanisms through which SARS-CoV-2 could impact the CNS during both the acute and recovery phases of infection and the potential selective vulnerability of PWH to these effects as a result of epidemiologic, clinical, and biologic factors. Finally, we define key research questions and considerations for the investigation of CNS sequelae of COVID-19 in PWH.


Subject(s)
COVID-19 , HIV Infections , Central Nervous System , Female , HIV Infections/complications , HIV Infections/epidemiology , Humans , Pandemics , Pregnancy , SARS-CoV-2
15.
Arq Neuropsiquiatr ; 79(11): 1049-1061, 2021 11.
Article in English | MEDLINE | ID: covidwho-1533456

ABSTRACT

The Scientific Department of Neuroimmunology of the Brazilian Academy of Neurology (DCNI/ABN) and Brazilian Committee for Treatment and Research in Multiple Sclerosis and Neuroimmunological Diseases (BCTRIMS) provide recommendations in this document for vaccination of the population with demyelinating diseases of the central nervous system (CNS) against infections in general and against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes COVID-19. We emphasize the seriousness of the current situation in view of the spread of COVID-19 in our country. Therefore, reference guides on vaccination for clinicians, patients, and public health authorities are particularly important to prevent some infectious diseases. The DCNI/ABN and BCTRIMS recommend that patients with CNS demyelinating diseases (e.g., MS and NMOSD) be continually monitored for updates to their vaccination schedule, especially at the beginning or before a change in treatment with a disease modifying drug (DMD). It is also important to note that vaccines are safe, and physicians should encourage their use in all patients. Clearly, special care should be taken when live attenuated viruses are involved. Finally, it is important for physicians to verify which DMD the patient is receiving and when the last dose was taken, as each drug may affect the induction of immune response differently.


Subject(s)
COVID-19 , Multiple Sclerosis , Neurology , Central Nervous System , Humans , Multiple Sclerosis/drug therapy , SARS-CoV-2 , Vaccination
16.
Curr Opin Pediatr ; 33(6): 597-602, 2021 12 01.
Article in English | MEDLINE | ID: covidwho-1501214

ABSTRACT

PURPOSE OF REVIEW: The purpose of this review is to address our current understanding of the pathophysiology of neurologic injury resulting from severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection on the developing nervous system. RECENT FINDINGS: SARS-CoV2 may enter the brain through three potential mechanisms: transsynaptic spread from the olfactory bulb following intranasal exposure, migration across the blood-brain barrier through endothelial cell infection, and migration following disruption of the blood-brain barrier from resulting inflammation. SARS-CoV2 does not appear to directly infect neurons but rather may produce an inflammatory cascade that results in neuronal injury. Additionally, autoantibodies targeting neuronal tissue resulting from the immune response to SARS-CoV2 are present in select patients and may contribute to central nervous system (CNS) injury. SUMMARY: These findings suggest that neuronal injury during SARS-CoV2 infection is immune mediated rather than through direct viral invasion. Further multimodal studies evaluating the pathophysiology of neurologic conditions in pediatric patients specifically following SARS-CoV2 infection are needed to improve our understanding of mechanisms driving neurologic injury and to identify potential treatment options.


Subject(s)
COVID-19 , Nervous System Diseases , Central Nervous System , Child , Humans , RNA, Viral , SARS-CoV-2
17.
J Neurovirol ; 27(6): 864-884, 2021 12.
Article in English | MEDLINE | ID: covidwho-1491452

ABSTRACT

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This virus, which was first identified in December 2019 in China, has resulted in a yet ongoing viral pandemic. Coronaviridae could potentially cause several disorders in a wide range of hosts such as birds and mammals. Although infections caused by this family of viruses are predominantly limited to the respiratory tract, Betacoronaviruses are potentially able to invade the central nervous system (CNS) as well as many other organs, thereby inducing neurological damage ranging from mild to lethal in both animals and humans. Over the past two decades, three novel CoVs, SARS-CoV-1, MERS-CoV, and SARS-CoV-2, emerging from animal reservoirs have exhibited neurotropic properties causing severe and even fatal neurological diseases. The pathobiology of these neuroinvasive viruses has yet to be fully known. Both clinical features of the previous CoV epidemics (SARS-CoV-1 and MERS-CoV) and lessons from animal models used in studying neurotropic CoVs, especially SARS and MERS, constitute beneficial tools in comprehending the exact mechanisms of virus implantation and in illustrating pathogenesis and virus dissemination pathways in the CNS. Here, we review the animal research which assessed CNS infections with previous more studied neurotropic CoVs to demonstrate how experimental studies with appliable animal models can provide scientists with a roadmap in the CNS impacts of SARS-CoV-2. Indeed, animal studies can finally help us discover the underlying mechanisms of damage to the nervous system in COVID-19 patients and find novel therapeutic agents in order to reduce mortality and morbidity associated with neurological complications of SARS-CoV-2 infection.


Subject(s)
COVID-19 , Middle East Respiratory Syndrome Coronavirus , Animals , Central Nervous System , Humans , Pandemics , SARS-CoV-2
18.
Exp Brain Res ; 240(1): 9-25, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1482199

ABSTRACT

The devastating COVID-19 pandemic is caused by the SARS-CoV-2 virus. It primarily affects the lung and induces acute respiratory distress leading to a decrease in oxygen supply to the cells. This lung insufficiency caused by SARS-CoV-2 virus contributes to hypoxia which can affect the brain and other organ systems. The heightened cytokine storm in COVID-19 patients leads to an immune reaction in the vascular endothelial cells that compromise the host defenses against the SARS-CoV-2 virus in various organs. The vascular endothelial cell membrane breach allows access for SARS-CoV-2 to infect multiple tissues and organs. The neurotropism of spike protein in SARS-CoV-2 rendered by furin site insertion may increase neuronal infections. These could result in encephalitis and encephalopathy. The COVID-19 patients suffered severe lung deficiency often showed effects in the brain and neural system. The early symptoms include headache, loss of smell, mental confusion, psychiatric disorders and strokes, and rarely encephalitis, which indicated the vulnerability of the nervous system to SARS-CoV-2. Infection of the brain and peripheral nervous system can lead to the dysfunction of other organs and result in multi-organ failure. This review focuses on discussing the vulnerability of the nervous system based on the pattern of expression of the receptors for the SARS-CoV-2 and the mechanisms of its cell invasion. The SARS-CoV-2 elicited immune response and host immune response evasion are further discussed. Then the effects on the nervous system and its consequences on neuro-sensory functions are discussed. Finally, the emerging information on the overall genetic susceptibility seen in COVID-19 patients and its implications for therapy outlook is discussed.


Subject(s)
COVID-19 , Nervous System Diseases , Stroke , Central Nervous System , Endothelial Cells , Humans , Pandemics , SARS-CoV-2
19.
J Stroke Cerebrovasc Dis ; 31(1): 106163, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1482759

ABSTRACT

The SARS-CoV-2 virus, which causes Coronavirus disease 2019 (COVID-19), has resulted in millions of worldwide deaths. When the SARS-CoV-2 virus emerged from Wuhan, China in December 2019, reports of patients with COVID-19 revealed that hospitalized patients had acute changes in mental status, cognition, and encephalopathy. Neurologic complications can be a consequence from overall severity of the systemic infection, direct viral invasion of the SARS-CoV-2 virus in the central nervous system, and possible immune mediated mechanisms. We will examine the landscape regarding this topic in this review in addition to current understandings of COVID-19 and hemostasis, treatment, and prevention, as well as vaccination.


Subject(s)
COVID-19 , Central Nervous System/virology , Nervous System Diseases , Thrombophilia/prevention & control , Anticoagulants , Hemostasis , Humans , Nervous System Diseases/diagnosis , Nervous System Diseases/etiology , SARS-CoV-2 , Thrombophilia/diagnosis
20.
Viruses ; 13(10)2021 10 17.
Article in English | MEDLINE | ID: covidwho-1471000

ABSTRACT

Coronavirus 2019 (COVID-19) is an infectious respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that mainly affects the lungs. COVID-19 symptoms include the presence of fevers, dry coughs, fatigue, sore throat, headaches, diarrhea, and a loss of taste or smell. However, it is understood that SARS-CoV-2 is neurotoxic and neuro-invasive and could enter the central nervous system (CNS) via the hematogenous route or via the peripheral nerve route and causes encephalitis, encephalopathy, and acute disseminated encephalomyelitis (ADEM) in COVID-19 patients. This review discusses the possibility of SARS-CoV-2-mediated Multiple Sclerosis (MS) development in the future, comparable to the surge in Parkinson's disease cases following the Spanish Flu in 1918. Moreover, the SARS-CoV-2 infection is associated with a cytokine storm. This review highlights the impact of these modulated cytokines on glial cell interactions within the CNS and their role in potentially prompting MS development as a secondary disease by SARS-CoV-2. SARS-CoV-2 is neurotropic and could interfere with various functions of neurons leading to MS development. The influence of neuroinflammation, microglia phagocytotic capabilities, as well as hypoxia-mediated mitochondrial dysfunction and neurodegeneration, are mechanisms that may ultimately trigger MS development.


Subject(s)
COVID-19/complications , COVID-19/pathology , Central Nervous System/pathology , Multiple Sclerosis/pathology , Neurodegenerative Diseases/virology , Central Nervous System/virology , Cytokine Release Syndrome/pathology , Cytokines/blood , Cytokines/metabolism , History, 20th Century , Humans , Influenza Pandemic, 1918-1919/statistics & numerical data , Multiple Sclerosis/virology , Neurodegenerative Diseases/pathology , SARS-CoV-2/immunology
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