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Journal articles on the topic 'Cytokine neuroinvasion'

Author: Grafiati

Published: 6 June 2025

Last updated: 25 July 2025

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1

Loskutov, O. A. "Neuroinvasion and neurological complications in COVID-19." Infusion & Chemotherapy, no. 3.2 (December 15, 2020): 186–87. http://dx.doi.org/10.32902/2663-0338-2020-3.2-186-187.

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Background. Coronavirus disease (COVID-19) affects not only the alveoli but also the central nervous system. The pathogenesis of neurological complications of COVID-19 is based on the receptor damage, cytokine-mediated injury, damage of the nervous system due to hypoxia, and neuronal damage due to the retrograde transport of the virus through nerve fibers. Objective. To determine the mechanisms of coronavirus neuroinvasion and treatment of neurological complications COVID-19. Materials and methods. Analysis of literature sources and own research on this topic. Results and dis

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2

Orandle, Marlene S., Andrew G. MacLean, Vito G. Sasseville, Xavier Alvarez, and Andrew A. Lackner. "Enhanced Expression of Proinflammatory Cytokines in the Central Nervous System Is Associated with Neuroinvasion by Simian Immunodeficiency Virus and the Development of Encephalitis." Journal of Virology 76, no. 11 (2002): 5797–802. http://dx.doi.org/10.1128/jvi.76.11.5797-5802.2002.

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ABSTRACT Inflammatory cytokines are believed to play an important role in the pathogenesis of human immunodeficiency virus type 1-associated encephalitis. To examine this in the simian immunodeficiency virus (SIV)-infected macaque model of neuroAIDS, inflammatory cytokine gene expression was evaluated in the brains of macaques infected with pathogenic SIVmac251 by reverse transcriptase PCR. Interleukin-1 beta was readily detected in the brains of all animals evaluated, regardless of infection status or duration of infection. Tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ) tran

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3

Freire-de-Lima, Leonardo, Aline Miranda Scovino, Leonardo Marques da Fonseca, et al. "COVID-19 Infection and Neuropathological Features." Medicines 8, no. 10 (2021): 59. http://dx.doi.org/10.3390/medicines8100059.

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The pathology associated with COVID-19 infection is progressively being revealed. Recent postmortem assessments have revealed acute airway inflammation as well as diffuse alveolar damage, which bears resemblance to severe acute respiratory syndromes induced by both SARS-CoV and MERS-CoV infections. Although recent papers have highlighted some neuropathologies associated with COVID-19 infection, little is known about this topic of great importance in the area of public health. Here, we discuss how neuroinflammation related to COVID-19 could be triggered by direct viral neuroinvasion and/or cyto

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4

Altable, Marcos, Moisés de la Serna Juan, Díaz-Moreno Emilio, Cruzado Alfonso, and Alvarez-Montano David. "Neuropsychiatry and COVID-19: An Overview." Neuropsychiatry 12, no. 1 (2023): 7. https://doi.org/10.37532/1758-2008.2022.12(1).615.

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Most of studies that exist on the COVID-19 pandemic produced by the SARS-CoV-2 coronavirus, report neuropsychiatric symptoms only as part of the manifestation of the disease in its terminal phase. However, there are neuropsychiatric symptoms since the beginning of the disease. Several investigations have indicated a direct relationship between chronic diseases such as Human Immunodeficiency Virus (HIV), tuberculosis, SARS, MERS, Ebola and SARS 2003 with mental disorders such as depression. Neuropsychiatric disorders can occur due to different mechanisms, such as cerebral hypoxia, cytokine stor

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5

Alexeeva, N. T., D. A. Sokolov, D. B. Nikityuk, S. V. Klochkova, and A. G. Kvaratskheliya. "Molecular and cellular mechanisms of central nervous system alteration in COVID-19." Journal of Anatomy and Histopathology 9, no. 3 (2020): 72–85. http://dx.doi.org/10.18499/2225-7357-2020-9-3-72-85.

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The ongoing coronavirus disease 2019 (COVID-19) pandemic dictates the need to study the molecular and cellular mechanisms of interaction between the pathogen and the human body. The manifestation of neurological symptoms in some patients with COVID-19 is a problem for neuroscientists due to the insufficiently understood pathomorphogenesis of the disease. This review systematizes the literature data reflecting the ways of penetration of SARS-CoV-2 into the brain, features of its interaction with neurons, neuroglia, and immune cells. It has been shown that the main mechanisms of SARS-CoV-2 neuro

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Gardner, Jameson K., та Melissa M. Herbst-Kralovetz. "IL-36γ regulates neutrophil infiltration and limits neuroinvasion in genital HSV-2 pathogenesis". Journal of Immunology 202, № 1_Supplement (2019): 75.5. http://dx.doi.org/10.4049/jimmunol.202.supp.75.5.

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Abstract Herpes simplex virus 2 is a neurotropic virus that causes a persistent, life-long infection that increases risk for other sexually transmitted infections. The vaginal epithelium is the first line of defense against HSV-2 and secretes immune mediators, including the pro-inflammatory cytokine IL-36γ, to coordinate the immune response. Previously, we showed that IL-36γ treatment promoted polymorphonuclear cell infiltration to the vaginal cavity and protected against lethal HSV-2 challenge. Herein, we extended these findings using flow cytometry to profile the cellular infiltrate. IL-36γ

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Freitas, Priscilla dos Santos Lieuthier, Ana Victória de Lima Lima, Karina Glazianne Barbosa Carvalho, et al. "Limbic Encephalitis Brain Damage Induced by Cocal Virus in Adult Mice Is Reduced by Environmental Enrichment: Neuropathological and Behavioral Studies." Viruses 13, no. 1 (2020): 48. http://dx.doi.org/10.3390/v13010048.

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We previously demonstrated, using the Piry virus model, that environmental enrichment promotes higher T-cell infiltration, fewer microglial changes, and faster central nervous system (CNS) virus clearance in adult mice. However, little is known about disease progression, behavioral changes, CNS cytokine concentration, and neuropathology in limbic encephalitis in experimental models. Using Cocal virus, we infected C57Bl6 adult mice and studied the neuroanatomical distribution of viral antigens in correlation with the microglial morphological response, measured the CNS cytokine concentration, an

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8

Zidovec-Lepej, Snjezana, Tatjana Vilibic-Cavlek, Ljubo Barbic, et al. "Antiviral Cytokine Response in Neuroinvasive and Non-Neuroinvasive West Nile Virus Infection." Viruses 13, no. 2 (2021): 342. http://dx.doi.org/10.3390/v13020342.

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Data on the immune response to West Nile virus (WNV) are limited. We analyzed the antiviral cytokine response in serum and cerebrospinal fluid (CSF) samples of patients with WNV fever and WNV neuroinvasive disease using a multiplex bead-based assay for the simultaneous quantification of 13 human cytokines. The panel included cytokines associated with innate and early pro-inflammatory immune responses (TNF-α/IL-6), Th1 (IL-2/IFN-γ), Th2 (IL-4/IL-5/IL-9/IL-13), Th17 immune response (IL-17A/IL-17F/IL-21/IL-22) and the key anti-inflammatory cytokine IL-10. Elevated levels of IFN-γ were detected in

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Aliyeva, M. B., S. S. Saparbayev, D. N. Ayaganov, M. S. Kurmangazin, and N. M. Tuychibaeva. "Neurological aspects of COVID-19." Kazan medical journal 102, no. 6 (2021): 877–86. http://dx.doi.org/10.17816/kmj2021-877.

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The coronavirus disease COVID-19 began to spread worldwide in December 2019 from the city of Wuhan (China). COVID-19 is often accompanied by fever, hypoxemic respiratory failure and systemic complications (for example, gastrointestinal, renal, cardiac, neurological, and hepatic lesions), thrombotic phenomena. Central nervous system damage is caused by the primary effect on it, direct neuroinvasion of the virus, and more often by secondary effect due to systemic hyperinflammation. Neurological manifestations include fatigue, headache, insomnia, and olfactory/taste disorders. Neurological manife

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10

Proenca-Modena, Jose Luiz, Jennifer L. Hyde, Renata Sesti-Costa, et al. "Interferon-Regulatory Factor 5-Dependent Signaling Restricts Orthobunyavirus Dissemination to the Central Nervous System." Journal of Virology 90, no. 1 (2015): 189–205. http://dx.doi.org/10.1128/jvi.02276-15.

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ABSTRACT Interferon (IFN)-regulatory factor 5 (IRF-5) is a transcription factor that induces inflammatory responses after engagement and signaling by pattern recognition receptors. To define the role of IRF-5 during bunyavirus infection, we evaluated Oropouche virus (OROV) and La Crosse virus (LACV) pathogenesis and immune responses in primary cells and in mice with gene deletions in Irf3 , Irf5 , and Irf7 or in Irf5 alone. Deletion of Irf3 , Irf5 , and Irf7 together resulted in uncontrolled viral replication in the liver and spleen, hypercytokinemia, extensive liver injury, and an early-death

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Schnekenberg, Luiz, Annahita Sedghi, Daniela Schoene, et al. "Assessment and Therapeutic Modulation of Heart Rate Variability: Potential Implications in Patients with COVID-19." Journal of Cardiovascular Development and Disease 10, no. 7 (2023): 297. http://dx.doi.org/10.3390/jcdd10070297.

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Cardiac damage has been attributed to SARS-CoV-2-related pathology contributing to increased risk of vascular events. Heart rate variability (HRV) is a parameter of functional neurocardiac integrity with low HRV constituting an independent predictor of cardiovascular mortality. Whether structural cardiac damage translates into neurocardiac dysfunction in patients infected with SARS-CoV-2 remains poorly understood. Hypothesized mechanisms of possible neurocardiac dysfunction in COVID-19 comprise direct systemic neuroinvasion of autonomic control centers, ascending virus propagation along crania

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Roy, B., and I. Banerjee. "Epileptic seizures in patients with COVID-19: A systematic review of early evidences." Journal of Biomedical Sciences 8, no. 1 (2021): 33–44. http://dx.doi.org/10.3126/jbs.v8i1.38459.

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Background: Global emergence of SARS-CoV-2 surfaced neurological complications amongst the patients. COVID-19 resembles with other coronavirus strains follows a trend of neurological complication, damage and encephalopathy, which entails considerable risks, requires attention for the neurologists. This is, to our knowledge, the first systematic review of the literature to investigate solely to elucidate the seizure spectrum by unfolding epileptogenicity of the SARS CoV-2 and potential pathways of neuroinvasion. Methods: A systematic literature search was performed in PubMed and Embase da

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Leng, Albert, Manuj Shah, Syed Ameen Ahmad, et al. "Pathogenesis Underlying Neurological Manifestations of Long COVID Syndrome and Potential Therapeutics." Cells 12, no. 5 (2023): 816. http://dx.doi.org/10.3390/cells12050816.

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The development of long-term symptoms of coronavirus disease 2019 (COVID-19) more than four weeks after primary infection, termed “long COVID” or post-acute sequela of COVID-19 (PASC), can implicate persistent neurological complications in up to one third of patients and present as fatigue, “brain fog”, headaches, cognitive impairment, dysautonomia, neuropsychiatric symptoms, anosmia, hypogeusia, and peripheral neuropathy. Pathogenic mechanisms of these symptoms of long COVID remain largely unclear; however, several hypotheses implicate both nervous system and systemic pathogenic mechanisms su

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14

Mutso, Margit, James A. St John, Zheng Lung Ling, et al. "Basic insights into Zika virus infection of neuroglial and brain endothelial cells." Journal of General Virology 101, no. 6 (2020): 622–34. http://dx.doi.org/10.1099/jgv.0.001416.

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Zika virus (ZIKV) has recently emerged as an important human pathogen due to the strong evidence that it causes disease of the central nervous system, particularly microcephaly and Guillain–Barré syndrome. The pathogenesis of disease, including mechanisms of neuroinvasion, may include both invasion via the blood–brain barrier and via peripheral (including cranial) nerves. Cellular responses to infection are also poorly understood. This study characterizes the in vitro infection of laboratory-adapted ZIKV African MR766 and two Asian strains of (1) brain endothelial cells (hCMEC/D3 cell line) an

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Mehwish Wazir, Muhammad Shakeel, and Tahira Batool. "A Review of Neurological Symptoms and Complication of Covid 19." Physical Education, Health and Social Sciences 3, no. 2 (2025): 126–36. https://doi.org/10.63163/jpehss.v3i2.250.

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The first case was identified in December 2019, the Human coronavirus disease 2019 (HCOV-19), caused by the severe acute respiratory syndrome coronavirus 2, spread quickly, resulting in a global pandemic. As of early 2025, the virus infected over 200 countries, with over 3.5 million cases and an estimated 165,000 to 243,000 fatalities. Largely characterized by respiratory and cardiovascular complications, recent studies highlight the wide-ranging effect of the virus on the nervous system. The neurological presentations range from mild manifestations, such as headache (in about 10–20% of patien

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Надіжко, Олена, and Svitlana Zubchenko. "IMMUNOLOGICAL FEATURES OF COVID-19 IN PATIENTS WITH NEUROPSYCHIATRIC SYMPTOMS AND HHV-6-INFECTION." Immunology and Allergology: Science and Practice, no. 4 (February 1, 2024): 12–22. http://dx.doi.org/10.37321/immunology.2023.4-02.

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SARS-CoV-2 infection in most cases is characterised by mild symptoms of fever, tiredness and dry cough. Coronaviruses can also induce cognitive, emotional, neurovegetative and behavioral dysregulation due to direct neurological injury through hypoxic damage and neuroinvasion. Most SARS-CoV-2 infections resolve within two weeks. However, the infection, which is characterized by neurological and neuropsychiatric symptoms, may last longer than 12 weeks. This phenomenon has been termed as Long COVID (LC) – a multisystemic condition, associated with acute phase disease severities. Several hypothese

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Benzarti, Emna, Kristy O. Murray, and Shannon E. Ronca. "Interleukins, Chemokines, and Tumor Necrosis Factor Superfamily Ligands in the Pathogenesis of West Nile Virus Infection." Viruses 15, no. 3 (2023): 806. http://dx.doi.org/10.3390/v15030806.

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West Nile virus (WNV) is a mosquito-borne pathogen that can lead to encephalitis and death in susceptible hosts. Cytokines play a critical role in inflammation and immunity in response to WNV infection. Murine models provide evidence that some cytokines offer protection against acute WNV infection and assist with viral clearance, while others play a multifaceted role WNV neuropathogenesis and immune-mediated tissue damage. This article aims to provide an up-to-date review of cytokine expression patterns in human and experimental animal models of WNV infections. Here, we outline the interleukin

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18

Dahm, Tobias, Henriette Rudolph, Christian Schwerk, Horst Schroten, and Tobias Tenenbaum. "Neuroinvasion and Inflammation in Viral Central Nervous System Infections." Mediators of Inflammation 2016 (2016): 1–16. http://dx.doi.org/10.1155/2016/8562805.

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Neurotropic viruses can cause devastating central nervous system (CNS) infections, especially in young children and the elderly. The blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) have been described as relevant sites of entry for specific viruses as well as for leukocytes, which are recruited during the proinflammatory response in the course of CNS infection. In this review, we illustrate examples of established brain barrier models, in which the specific reaction patterns of different viral families can be analyzed. Furthermore, we highlight the pathogen specific

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Bleau, Christian, Aveline Filliol, Michel Samson, and Lucie Lamontagne. "Brain Invasion by Mouse Hepatitis Virus Depends on Impairment of Tight Junctions and Beta Interferon Production in Brain Microvascular Endothelial Cells." Journal of Virology 89, no. 19 (2015): 9896–908. http://dx.doi.org/10.1128/jvi.01501-15.

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ABSTRACTCoronaviruses (CoVs) have shown neuroinvasive properties in humans and animals secondary to replication in peripheral organs, but the mechanism of neuroinvasion is unknown. The major aim of our work was to evaluate the ability of CoVs to enter the central nervous system (CNS) through the blood-brain barrier (BBB). Using the highly hepatotropic mouse hepatitis virus type 3 (MHV3), its attenuated variant, 51.6-MHV3, which shows low tropism for endothelial cells, and the weakly hepatotropic MHV-A59 strain from the murine coronavirus group, we investigated the virus-induced dysfunctions of

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Lino, Allison, Timothy A. Erickson, Melissa S. Nolan, Kristy O. Murray, and Shannon E. Ronca. "A Preliminary Study of Proinflammatory Cytokines and Depression Following West Nile Virus Infection." Pathogens 11, no. 6 (2022): 650. http://dx.doi.org/10.3390/pathogens11060650.

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West Nile virus (WNV) is a neurotropic flavivirus that can cause acute febrile illness leading to neuroinvasive disease. Depression is a well-described outcome following infection, but the underlying pathogenic mechanisms are unknown. Proinflammatory cytokines play important roles in WNV infection, but their role in depression post-WNV remains unstudied. This research aimed to retrospectively evaluate associations between proinflammatory cytokines and new onset depression in a WNV cohort. Participants with asymptomatic WNV infection were significantly less likely to report new onset depression

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21

Vilibic-Cavlek, Tatjana, Snjezana Zidovec-Lepej, Dragan Ledina, et al. "Clinical, Virological, and Immunological Findings in Patients with Toscana Neuroinvasive Disease in Croatia: Report of Three Cases." Tropical Medicine and Infectious Disease 5, no. 3 (2020): 144. http://dx.doi.org/10.3390/tropicalmed5030144.

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Toscana virus (TOSV) is an arthropod-borne virus, transmitted to humans by phlebotomine sandflies. Although the majority of infections are asymptomatic, neuroinvasive disease may occur. We report three cases of neuroinvasive TOSV infection detected in Croatia. Two patients aged 21 and 54 years presented with meningitis, while a 22-year old patient presented with meningoencephalitis and right-sided brachial plexitis. Cerebrospinal fluid (CSF), serum, and urine samples were collected and tested for neuroinvasive arboviruses: tick-borne encephalitis, West Nile, Usutu, TOSV, Tahyna, and Bhanja vir

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Muniz, Mireya G. Ramos, and Charles T. Spencer. "A novel neuroinvasive infection modality for Francisella tularensis elicits neuroinflammation resulting in cellular damage." Journal of Immunology 204, no. 1_Supplement (2020): 67.21. http://dx.doi.org/10.4049/jimmunol.204.supp.67.21.

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Abstract Francisella tularensis (Ft.) is a gram-negative coccobacillus bacterium that causes the zoonotic disease tularemia in humans. Ft. causes the most severe form of the disease through inhalation, but is most commonly transmitted through direct contact with infected animal carcasses such as rodents and rabbits. Due to its extremely low infectious dose, high mortality rate, and potential use as a biological warfare agent, Ft. is classified by the CDC as a Tier 1 select agent. Ft. infection triggers an overactive inflammatory response, termed a “cytokine storm”, which produces excessive tis

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Constant, Orianne, Jonathan Barthelemy, Anna Nagy, Sara Salinas, and Yannick Simonin. "West Nile Virus Neuroinfection in Humans: Peripheral Biomarkers of Neuroinflammation and Neuronal Damage." Viruses 14, no. 4 (2022): 756. http://dx.doi.org/10.3390/v14040756.

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Among emerging arthropod-borne viruses (arbovirus), West Nile virus (WNV) is a flavivirus that can be associated with severe neuroinvasive infections in humans. In 2018, the European WNV epidemic resulted in over 2000 cases, representing the most important arboviral epidemic in the European continent. Characterization of inflammation and neuronal biomarkers released during WNV infection, especially in the context of neuronal impairments, could provide insight into the development of predictive tools that could be beneficial for patient outcomes. We first analyzed the inflammatory signature in

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Hansen, Michael, Melissa S. Nolan, Rodion Gorchakov, Rodrigo Hasbun, Kristy O. Murray, and Shannon E. Ronca. "Unique Cytokine Response in West Nile Virus Patients Who Developed Chronic Kidney Disease: A Prospective Cohort Study." Viruses 13, no. 2 (2021): 311. http://dx.doi.org/10.3390/v13020311.

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West Nile virus (WNV) is a widespread and devastating disease, especially in those who develop neuroinvasive disease. A growing body of evidence describes sequelae years after infection, including neurological complications and chronic kidney disease (CKD). Eighty-nine out of 373 WNV-positive cases were followed for approximately two years and compared to 127 WNV-negative controls with and without CKD. Adjusted risk ratios (aRRs) were calculated via a log binomial regression to determine the impact of WNV exposure and other possible confounders on the likelihood of developing CKD. Cytokine pro

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James, Eddie, Theresa Gates, Duy May, Rebecca LaFond, Uma Malhotra, and William Kwok. "Quantitative and qualitative differences in CD4+ T cell responses for subjects with symptomatic and asymptomatic West Nile virus infection (P6125)." Journal of Immunology 190, no. 1_Supplement (2013): 173.16. http://dx.doi.org/10.4049/jimmunol.190.supp.173.16.

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Abstract The West Nile virus (WNV), a mosquito-borne flavivirus, induces a wide range of clinical manifestations in humans. While the majority of infections are essentially asymptomatic, a small percentage of inflections lead to neuroinvasive disease with symptoms ranging from mild disorientation to paralysis and death. Increased risk of symptomatic infection in immunosuppressed subjects could suggest that lack of effective immune responses against WNV may lead to worse outcomes. In this study, we utilized HLA class II tetramers to characterize the epitope specificity, frequency, and phenotype

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Pavesi, Alessandro, Giorgio Tiecco, Luca Rossi, et al. "Inflammatory Response Associated with West Nile Neuroinvasive Disease: A Systematic Review." Viruses 16, no. 3 (2024): 383. http://dx.doi.org/10.3390/v16030383.

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Background: West Nile virus (WNV) infection is a seasonal arbovirosis with the potential to cause severe neurological disease. Outcomes of the infection from WNV depend on viral factors (e.g., lineage) and host-intrinsic factors (e.g., age, sex, immunocompromising conditions). Immunity is essential to control the infection but may also prove detrimental to the host. Indeed, the persistence of high levels of pro-inflammatory cytokines and chemokines is associated with the development of blood–brain barrier (BBB) damage. Due to the importance of the inflammatory processes in the development of W

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Stonedahl, Sarah, Penny Clarke, and Kenneth L. Tyler. "The Role of Microglia during West Nile Virus Infection of the Central Nervous System." Vaccines 8, no. 3 (2020): 485. http://dx.doi.org/10.3390/vaccines8030485.

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Encephalitis resulting from viral infections is a major cause of hospitalization and death worldwide. West Nile Virus (WNV) is a substantial health concern as it is one of the leading causes of viral encephalitis in the United States today. WNV infiltrates the central nervous system (CNS), where it directly infects neurons and induces neuronal cell death, in part, via activation of caspase 3-mediated apoptosis. WNV infection also induces neuroinflammation characterized by activation of innate immune cells, including microglia and astrocytes, production of inflammatory cytokines, breakdown of t

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Kumari, Pratima, Hussin A. Rothan, Janhavi P. Natekar, et al. "Neuroinvasion and Encephalitis Following Intranasal Inoculation of SARS-CoV-2 in K18-hACE2 Mice." Viruses 13, no. 1 (2021): 132. http://dx.doi.org/10.3390/v13010132.

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Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection can cause neurological disease in humans, but little is known about the pathogenesis of SARS-CoV-2 infection in the central nervous system (CNS). Herein, using K18-hACE2 mice, we demonstrate that SARS-CoV-2 neuroinvasion and encephalitis is associated with mortality in these mice. Intranasal infection of K18-hACE2 mice with 105 plaque-forming units of SARS-CoV-2 resulted in 100% mortality by day 6 after infection. The highest virus titers in the lungs were observed on day 3 and declined on days 5 and 6 after infection. By c

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Halasah, Nadeem, Isha Kallingal, and Douglas Durrant. "IL-10 mitigates inflammation within the CNS during West Nile virus neuroinvasive disease." Journal of Immunology 212, no. 1_Supplement (2024): 1244_5936. http://dx.doi.org/10.4049/jimmunol.212.supp.1244.5936.

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Abstract West Nile virus (WNV) causes a severe CNS infection in humans, primarily in the elderly and immunocompromised. Prior studies revealed that IL-10, primarily through the suppression of antiviral and proinflammatory cytokine production, predominately has a negative role in WNV immunity. However, in the absence of a critical DC-subset, IL-10-expressing lymphocyte infiltration was reduced in the WNV-infected CNS and excessive inflammation and immunopathology caused increased susceptibility to WNND. These results suggest a neuroprotective role of IL-10. Preliminary findings demonstrate CD8+

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Radkowski, Marek, Tomasz Kryczka, Bogna Szymańska-Kotwica, et al. "Depression and Cognitive Dysfunction in Patients with Chronic Hepatitis C: Correlation with Viral Replication in the Peripheral Blood Mononuclear Cells and Cytokines in Serum." International Journal of Molecular Sciences 24, no. 20 (2023): 15351. http://dx.doi.org/10.3390/ijms242015351.

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Chronic hepatitis C virus (HCV) infection is commonly associated with depression and cognitive dysfunction, the cause of which could be related to the HCV neuroinvasion and/or state of chronic inflammation. Viral sequences and proteins were previously detected in the brain and since blood leukocytes can cross the blood–brain barrier, they could provide viral access to the CNS. Eighty chronic hepatitis C patients were tested for viral replication in PBMCs (detection of the HCV RNA-negative strand) and serum cytokines. Depression was assessed by the Beck Depression Inventory (BDI), neuroticism b

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Graham, Jessica B., Jessica Swarts, Sunil Thomas, et al. "West Nile virus infection in the Collaborative Cross mouse model recapitulates unique human disease states." Journal of Immunology 196, no. 1_Supplement (2016): 79.11. http://dx.doi.org/10.4049/jimmunol.196.supp.79.11.

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Abstract West Nile Virus (WNV) is a cytopathic neurotropic flavivirus that causes a wide range of infection states in humans, ranging from asymptomatic to severe neuroinvasive disease. This variation supports the idea that host genetics play an important role in immunity to WNV infection. The significant individual to individual variation in immune responses within the human population can not be fully captured in single laboratory inbred strains, so a systems genetic approach requires the use of the Collaborative Cross (CC) mouse system to identify polymorphic host genes and networks that con

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Manosso, Luana M., Camila O. Arent, Laura A. Borba, Luciane B. Ceretta, João Quevedo, and Gislaine Z. Réus. "Microbiota-Gut-Brain Communication in the SARS-CoV-2 Infection." Cells 10, no. 8 (2021): 1993. http://dx.doi.org/10.3390/cells10081993.

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The coronavirus disease of 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome 2 (SARS-CoV-2). In addition to pneumonia, individuals affected by the disease have neurological symptoms. Indeed, SARS-CoV-2 has a neuroinvasive capacity. It is known that the infection caused by SARS-CoV-2 leads to a cytokine storm. An exacerbated inflammatory state can lead to the blood–brain barrier (BBB) damage as well as to intestinal dysbiosis. These changes, in turn, are associated with microglial activation and reactivity of astrocytes that can promote the degeneration of neu

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Kalergis, Alexis M., Karen bohmwald, and Catalina A. Andrade. "Pneumoviruses can impair the central nervous system by different mechanisms." Journal of Immunology 210, no. 1_Supplement (2023): 236.22. http://dx.doi.org/10.4049/jimmunol.210.supp.236.22.

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Abstract Pneumoviruses such as the respiratory syncytial virus (hRSV) and the human metapneumovirus (hMPV) are the leading cause of acute lower tract respiratory infection, mainly in infants, elderly and immunocompromised individuals, causing high morbidity and mortality rates. However, these viruses can cause neurological alterations, such as encephalitis and encephalopathy. Viral RNA and pro-inflammatory molecules have been found in patients with neurological signs, supporting the notion of neuroinvasion and/or neuroinflammation caused by hRSV and hMPV. Therefore, this work seeks to evaluate

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Cente, Martin, Monika Danchenko, Ludovit Skultety, Peter Filipcik, and Zuzana Sekeyova. "Rickettsia Deregulates Genes Coding for the Neurotoxic Cell Response Pathways in Cerebrocortical Neurons In Vitro." Cells 12, no. 9 (2023): 1235. http://dx.doi.org/10.3390/cells12091235.

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Rickettsial infections of the central nervous system (CNS) are manifested by severe neurological symptoms and represent a serious life-threatening condition. Despite the considerable health danger, only a few studies have been conducted focusing on the pathogenesis induced by Rickettsia sp. in CNS. To investigate the signaling pathways associated with the neurotoxic effects of rickettsiae, we employed an experimental model of cerebrocortical neurons combined with molecular profiling and comprehensive bioinformatic analysis. The cytopathic effect induced by Rickettsia akari and Rickettsia slova

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Prančlová, Veronika, Václav Hönig, Marta Zemanová, Daniel Růžek, and Martin Palus. "Robust CXCL10/IP-10 and CCL5/RANTES Production Induced by Tick-Borne Encephalitis Virus in Human Brain Pericytes Despite Weak Infection." International Journal of Molecular Sciences 25, no. 14 (2024): 7892. http://dx.doi.org/10.3390/ijms25147892.

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Tick-borne encephalitis virus (TBEV) targets the central nervous system (CNS), leading to potentially severe neurological complications. The neurovascular unit plays a fundamental role in the CNS and in the neuroinvasion of TBEV. However, the role of human brain pericytes, a key component of the neurovascular unit, during TBEV infection has not yet been elucidated. In this study, TBEV infection of the primary human brain perivascular pericytes was investigated with highly virulent Hypr strain and mildly virulent Neudoerfl strain. We used Luminex assay to measure cytokines/chemokines and growth

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Dąbrowska, Eliza, Beata Galińska-Skok, and Napoleon Waszkiewicz. "Depressive and Neurocognitive Disorders in the Context of the Inflammatory Background of COVID-19." Life 11, no. 10 (2021): 1056. http://dx.doi.org/10.3390/life11101056.

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The dysfunctional effects of the coronavirus disease 2019 (COVID-19) infection on the nervous system are established. The manifestation of neuropsychiatric symptoms during and after infection is influenced by the neuroinvasive and neurotrophic properties of SARS-CoV-2 as well as strong inflammation characterised by a specific “cytokine storm”. Research suggests that a strong immune response to a SARS-CoV-2 infection and psychological stressors related to the pandemic may cause chronic inflammatory processes in the body with elevated levels of inflammatory markers contributing to the intensific

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Herzler, Joshua, Douglas Durrant, and Valeria Hernandez. "Targeting the NS4b Antigen of West Nile Virus to the Endocytic Receptor DEC-205 to Stimulate Protective T Cell Responses to West Nile Virus Encephalitis." Journal of Immunology 212, no. 1_Supplement (2024): 1301_5835. http://dx.doi.org/10.4049/jimmunol.212.supp.1301.5835.

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Abstract West Nile Virus (WNV), the primary cause of mosquito-borne neuroinvasive disease in the US, poses a significant public health threat without an approved human vaccine. DCs are pivotal in orchestrating immune responses, dictating antigen-specific effector T cell activation or tolerance based on their maturity. The endocytic receptor DEC-205, expressed by specific DC subsets, facilitates antigen uptake, processing, and cross-presentation, initiating an effective T cell response. Studies highlight DEC-205+ DCs within the CNS in reactivating antiviral effector T cell responses, restrictin

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Kundu, Gopen Kumar, F. Rabin, ER Nandi, Naveen Sheikh, and Shaheen Akhter. "Etiology and Risk Factors of Febrile Seizure An Update." Bangladesh Journal of Child Health 34, no. 3 (2012): 103–12. http://dx.doi.org/10.3329/bjch.v34i3.10361.

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Febrile seizures (FS) are the most common convulsive event in children. This condition has been described since the time of Hippocrates. The etiology of the febrile seizures are still unclear. In FS, there is a strong familial predisposition. This does not exclude infections as a causative factor because subtle genetic polymorphisms have been demonstrated to affect the course of infections. In an earlier review of the world literature (1924-1964), except for roseola infantum, viral infections as a cause of febrile seizures were rarely diagnosed. Reports of viral infections in the etiology of f

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Rai, Sachchida Nand, Neeraj Tiwari, Payal Singh, et al. "Exploring the Paradox of COVID-19 in Neurological Complications with Emphasis on Parkinson’s and Alzheimer’s Disease." Oxidative Medicine and Cellular Longevity 2022 (August 31, 2022): 1–16. http://dx.doi.org/10.1155/2022/3012778.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a human coronavirus (HCoV) that has created a pandemic situation worldwide as COVID-19. This virus can invade human cells via angiotensin-converting enzyme 2 (ACE2) receptor-based mechanisms, affecting the human respiratory tract. However, several reports of neurological symptoms suggest a neuroinvasive development of coronavirus. SARS-CoV-2 can damage the brain via several routes, along with direct neural cell infection with the coronavirus. The chronic inflammatory reactions surge the brain with proinflammatory elements, damagin

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Dedoni, Simona, Valeria Avdoshina, Chiara Camoglio, et al. "K18- and CAG-hACE2 Transgenic Mouse Models and SARS-CoV-2: Implications for Neurodegeneration Research." Molecules 27, no. 13 (2022): 4142. http://dx.doi.org/10.3390/molecules27134142.

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COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global pandemic that might lead to very serious consequences. Notably, mental status change, brain confusion, and smell and taste disorders along with neurological complaints have been reported in patients infected with SARS-CoV-2. Furthermore, human brain tissue autopsies from COVID-19 patients show the presence of SARS-CoV-2 neuroinvasion, which correlates with the manifestation of meningitis, encephalitis, leukocyte infiltration, and neuronal damage. The olfactory mucosa has been suggested as a way of ent

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Ryman, Kate D., William B. Klimstra, Khuong B. Nguyen, Christine A. Biron, and Robert E. Johnston. "Alpha/Beta Interferon Protects Adult Mice from Fatal Sindbis Virus Infection and Is an Important Determinant of Cell and Tissue Tropism." Journal of Virology 74, no. 7 (2000): 3366–78. http://dx.doi.org/10.1128/jvi.74.7.3366-3378.2000.

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ABSTRACT Infection of adult 129 Sv/Ev mice with consensus Sindbis virus strain TR339 is subclinical due to an inherent restriction in early virus replication and viremic dissemination. By comparing the pathogenesis of TR339 in 129 Sv/Ev mice and alpha/beta interferon receptor null (IFN-α/βR−/−) mice, we have assessed the contribution of IFN-α/β in restricting virus replication and spread and in determining cell and tissue tropism. In adult 129 Sv/Ev mice, subcutaneous inoculation with 100 PFU of TR339 led to extremely low-level virus replication and viremia, with clearance under way by 96 h po

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Askovic, Srdjan, Cynthia Favara, Frank J. McAtee та John L. Portis. "Increased Expression of MIP-1α and MIP-1β mRNAs in the Brain Correlates Spatially and Temporally with the Spongiform Neurodegeneration Induced by a Murine Oncornavirus". Journal of Virology 75, № 6 (2001): 2665–74. http://dx.doi.org/10.1128/jvi.75.6.2665-2674.2001.

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ABSTRACT The chimeric murine oncornavirus FrCasE causes a rapidly progressive paralytic disease associated with spongiform neurodegeneration throughout the neuroaxis. Neurovirulence is determined by the sequence of the viral envelope gene and by the capacity of the virus to infect microglia. The neurocytopathic effect of this virus appears to be indirect, since the cells which degenerate are not infected. In the present study we have examined the possible role of inflammatory responses in this disease and have used as a control the virus F43. F43 is an highly neuroinvasive but avirulent virus

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Cavalcante, Maria Sueli Barbosa, Diego Siqueira Santos, Lidineuza Machado Araújo, et al. "Inflammatory and neuropathological responses to Vesiculovirus carajas encephalitis in adult mice: variability, tolerance and resistance." Frontiers in Cellular and Infection Microbiology 15 (February 26, 2025). https://doi.org/10.3389/fcimb.2025.1499658.

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Vesiculovirus carajas (CARV) is a pathogen with neuroinvasive potential, yet its impact on neuroinflammation and sickness behavior remains poorly understood. In this study, we investigated the neuropathological and immunological responses to CARV encephalitis in adult BALB/c mice. Mice were intranasally inoculated with either infected or uninfected brain homogenates, and clinical, histopathological, and cytokine profiles were analyzed. CARV antigens were primarily detected in necrotic neurons, with prominent microglial activation near the ventricles and blood vessels. By day 10 post-infection,

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Song, Ren, Orkide O. Koyuncu, Todd M. Greco, Benjamin A. Diner, Ileana M. Cristea, and Lynn W. Enquist. "Two Modes of the Axonal Interferon Response Limit Alphaherpesvirus Neuroinvasion." mBio 7, no. 1 (2016). http://dx.doi.org/10.1128/mbio.02145-15.

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ABSTRACT Infection by alphaherpesviruses, including herpes simplex virus (HSV) and pseudorabies virus (PRV), typically begins at epithelial surfaces and continues into the peripheral nervous system (PNS). Inflammatory responses are induced at the infected peripheral site prior to invasion of the PNS. When the peripheral tissue is first infected, only the innervating axons are exposed to this inflammatory milieu, which includes the interferons (IFNs). The fundamental question is how do PNS cell bodies respond to these distant, potentially damaging events experienced by axons. Using compartmente

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Soung, Allison L., Abigail Vanderheiden, Anna S. Nordvig, et al. "COVID-19 induces CNS cytokine expression and loss of hippocampal neurogenesis." Brain, August 25, 2022. http://dx.doi.org/10.1093/brain/awac270.

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Abstract Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with acute and postacute cognitive and neuropsychiatric symptoms including impaired memory, concentration, attention, sleep and affect. Mechanisms underlying these brain symptoms remain understudied. Here we report that SARS-CoV-2-infected hamsters exhibit a lack of viral neuroinvasion despite aberrant blood–brain barrier permeability. Hamsters and patients deceased from coronavirus disease 2019 (COVID-19) also exhibit microglial activation and expression of interleukin (IL)-1β and IL-6, espe

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Waindok, Patrick, and Christina Strube. "Neuroinvasion of Toxocara canis- and T. cati-larvae mediates dynamic changes in brain cytokine and chemokine profile." Journal of Neuroinflammation 16, no. 1 (2019). http://dx.doi.org/10.1186/s12974-019-1537-x.

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Bouças, Ana P., Jakeline Rheinheimer, and Jim Lagopoulos. "Why Severe COVID-19 Patients Are at Greater Risk of Developing Depression: A Molecular Perspective." Neuroscientist, November 2, 2020, 107385842096789. http://dx.doi.org/10.1177/1073858420967892.

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The prevailing evidence suggests that patients with severe COVID-19 seem to have an overreaction of the immune system demonstrating exacerbated levels of inflammation caused by a “cytokine storm.” At this early stage, the mechanisms underpinning COVID-19 are still subject to intense scrutiny and the long-term mental health consequences as a result of the disease are unknown. Here we discuss the hypothesis that patients who survive severe COVID-19 and who experience significant activation of the immune system, are at greater risk of developing depression. We posit that a phenomenon known as cyt

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Meuren, Lana Monteiro, Elisa Beatriz Prestes, Michelle Premazzi Papa, et al. "Infection of Endothelial Cells by Dengue Virus Induces ROS Production by Different Sources Affecting Virus Replication, Cellular Activation, Death and Vascular Permeability." Frontiers in Immunology 13 (February 2, 2022). http://dx.doi.org/10.3389/fimmu.2022.810376.

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Exacerbated inflammatory response and altered vascular function are hallmarks of dengue disease. Reactive oxygen species (ROS) production has been associated to endothelial barrier disturbance and microvascular alteration in distinct pathological conditions. Increased ROS has been reported in in vitro models of dengue virus (DENV) infection, but its impact for endothelial cell physiology had not been fully investigated. Our group had previously demonstrated that infection of human brain microvascular endothelial cells (HBMEC) with DENV results in the activation of RNA sensors and production of

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Keshtgar, Zahra, GH Reza Chalabianloo, and Niloofar Esmaeili. "Probable Neuropsychological & Cognitive Complications due to Cytokine Storm in Patients With COVID-19." Basic and Clinical Neuroscience Journal, December 4, 2021, 1–37. http://dx.doi.org/10.32598/bcn.2022.3202.1.

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Introduction: COVID-19 (coronavirus disease 2019) was identified in China in December 2019 for the first time and is rapidly spreading throughout the world as a pandemic. As COVID-19 causes mild to severe acute respiratory syndrome, most studies in this context have focused on pathogenesis primarily in the respiratory system. However, evidence shows that the central nervous system (CNS) may also be affected by COVID-19. Since COVID-19 is spreading, it is imperative to study its possible cognitive effects in patients suffering and recovering from COVID-19. Methods: The articles used in this stu

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Tian, Debin, Wen Li, C. Lynn Heffron, et al. "Hepatitis E virus infects brain microvascular endothelial cells, crosses the blood–brain barrier, and invades the central nervous system." Proceedings of the National Academy of Sciences 119, no. 24 (2022). http://dx.doi.org/10.1073/pnas.2201862119.

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Hepatitis E virus (HEV) is an important but understudied zoonotic virus causing both acute and chronic viral hepatitis. A proportion of HEV-infected individuals also developed neurological diseases such as Guillain–Barré syndrome, neuralgic amyotrophy, encephalitis, and myelitis, although the mechanism remains unknown. In this study, by using an in vitro blood–brain barrier (BBB) model, we first investigated whether HEV can cross the BBB and whether the quasi-enveloped HEV virions are more permissible to the BBB than the nonenveloped virions. We found that both quasi-enveloped and nonenveloped

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