Relevant bibliographies by topics / Cytokine neuroinvasion

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Cytokine neuroinvasion'

Author: Grafiati
Published: 6 June 2025
Last updated: 25 July 2025

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Journal articles on the topic "Cytokine neuroinvasion"

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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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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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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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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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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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6

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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Dissertations / Theses on the topic "Cytokine neuroinvasion"

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"Regulation and Function of IL-36γ in Genital HSV-2 Infection and Disease Pathogenesis". Doctoral diss., 2019. http://hdl.handle.net/2286/R.I.55502.

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abstract: An estimated 267 million women worldwide are HSV-2 seropositive, including roughly 20% of reproductive-aged American women. HSV-2 is a neurotropic virus that establishes a persistent, life-long infection that increases risk for STI acquisition in individuals. The vaginal epithelium represents a critical first line of defense against infection, and during acute infection, underlying immune mechanisms in the epithelium may be critical to protect against disease pathogenesis. The recently identified pro-inflammatory cytokine IL-36gamma has been shown to be expressed at mucosal epithelia
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Book chapters on the topic "Cytokine neuroinvasion"

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Kumar Chatterjee, Swapan, Snigdha Saha, and Shahin Muhammed T.K. "COVID-19 and Its Impact on Onset and Progression of Parkinson’s and Cognitive Dysfunction." In COVID-19 Pandemic, Mental Health and Neuroscience - New Scenarios for Understanding and Treatment [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.105667.

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In the COVID-19 pandemic, neurological complications have emerged as a significant cause of morbidity and mortality. A wide range of neurological manifestations ranging from cognitive or memory disturbances, headache, loss of smell or taste, confusion, and disabling strokes have been reported during and post COVID conditions. The COVID-19 virus can utilize two possible pathways for invasion into the brain, either through retrograde axonal transport (olfactory route) or by crossing the blood-brain barrier (BBB). Furthermore, the production of SARS-CoV-2-associated cytokines, such as interleukin
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Conference papers on the topic "Cytokine neuroinvasion"

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Nunes, Alícia Malta Brandão. "COVID-19 and neuroinvasion: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.747.

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Background: Clinical practice throughout the pandemic has generated a debate about the existence of neurotropism and the neuropathogenic capacity of the new coronavirus. Medical professionals have noted that there is a wide spectrum of neurological manifestations associated with SARS-CoV-2 infections; from hyposmia to encephalopathy. The interaction of the viral protein spike (S) with the ACE2 gene present in endothelial and nerve cells and the cytokine storm triggered by COVID-19 are explanatory bases for a series of mechanisms proposed in recent literature. Objectives: To establish a direct
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Journal articles
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