Littérature scientifique sur le sujet « Cytokine neuroinvasion »
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Articles de revues sur le sujet "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.
Texte intégralRésumé :
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 discussion. In 3 days after infection viral antigens are detected in the olfactory sensory neurons of the nasal cavity epithelium, which confirms the transnasal invasion of coronaviruses. According to various authors, 36.4-84 % of patients with COVID-19 have neurological manifestations. In general, neurological symptoms of COVID-19 can be divided into three categories: symptoms of the central nervous system disorders (headache, dizziness, consciousness disorders, nausea and vomiting, ataxia, acute cerebrovascular disease, and epilepsy), symptoms of the peripheral nervous system disorders (hypogeusia, hyposmia, hypopsia, and neuralgia) and musculoskeletal symptoms. As viral infections cause cytokine storm, inflammation and hyperactive oxidation, it is advisable to use antioxidants in their treatment. According to the Japanese clinical guidelines for the treatment of acute respiratory distress syndrome, edaravone may be used as a free radical scavenger in such patients. In the experiment, edaravone reduced the area of infarction and promoted functional recovery in cerebral thrombosis. Other properties of edaravone include the prevention of excessive permeability of the pulmonary vessels’ endothelium. Own research has shown that edaravone (Ksavron, “Yuria-Pharm”) reduces the severity of inflammation and mortality in patients with COVID-19. In the control group, the level of the proinflammatory mediator interleukin-6 exceeded the upper limit of normal values by 1652.40 %, and in the Ksavron group – only by 269.97 %. Mortality in the control group was 14.3 %, and in the Ksavron group – 0 %.
 Conclusions. 1. Coronaviruses affect not only the lungs but also the nervous system. 2. Neurological symptoms of COVID-19 include headache, dizziness, consciousness disorders, nausea and vomiting, ataxia, acute cerebrovascular disease, hypogeusia, hyposmia, hypopsia, neuralgia, and musculoskeletal symptoms. 3. Edaravone (Ksavron) reduces the severity of inflammation and has an antioxidant effect, which justifies its use in COVID-19.
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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.
Texte intégralRésumé :
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) transcripts were undetectable in the brains of uninfected control animals but were upregulated at 7 and 14 days postinoculation. At the terminal stage of infection, TNF-α and IFN-γ transcripts were coexpressed in the brains of four of five animals with SIV encephalitis (SIVE). Within an encephalitic brain, TNF-α and IFN-γ transcripts were detected in six of seven regions with histologic evidence of SIVE, suggesting a direct relationship between neuropathology and altered cytokine gene expression. With combined fluorescent in situ hybridization and immunofluorescence, TNF-α-expressing cells were frequently identified as CD68-positive macrophages within perivascular lesions. These observations provide evidence that cytokines produced by activated inflammatory macrophages are an important element in the pathogenesis of SIVE.
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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.
Texte intégralRésumé :
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 cytokine release over the course of the infection.
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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.
Texte intégralRésumé :
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 storm due to exaggerated immune response and encephalitis due to direct brain infection. Nervous system involvement leads to poor prognosis of COVID-19.
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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.
Texte intégralRésumé :
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 neuroinvasion are presumably retrograde axonal transport along the fibers of the olfactory and vagus nerves; penetration through the damaged blood-brain barrier (BBB) or migration of immunocompetent cells containing viral particles through the intact BBB. It was found that virusinducible neuronal death is caused not only by a direct cytotoxic effect, but also due to dysregulation of the reninangiotensin system of the brain and the release of a large amount of inflammatory cytokines as a manifestation of a “cytokine storm”. The participation of neuroglial cells in the initiation and maintenance of neuroinflammatory and neurodegenerative processes due to the activation of their proinflammatory phenotype has been demonstrated. The role of mast cells in antiviral defense mechanisms and inflammatory reactions is discussed.
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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.
Texte intégralRésumé :
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 significantly (p < 0.0001) induced transient neutrophil infiltration, but did not impact monocyte or macrophage recruitment. Using IL-36γ−/− mice in a lethal HSV-2 challenge model, we show that neutrophils were significantly (p < 0.0001) depleted at 1- and 2-days post infection, and that mature neutrophil recruitment was impaired. In addition, IL-36γ−/− mice develop genital disease more rapidly (p < 0.0001), have significantly (p < 0.0001) reduced survival time, and display an increased incidence (p < 0.0001) of neurologic disease compared to wild type mice. IL-36γ−/− mice exhibited a significant (p < 0.05) delay in clearance of the virus from the vaginal epithelium, and analysis of virus spread to the spinal cord, bladder, and colon demonstrated that HSV-2 spread significantly (p < 0.05) more quickly in IL-36γ−/− mice. Further, we detected productive HSV-2 infection in the brainstem of IL-36γ−/− mice significantly (p < 0.0001) more frequently than in wild type mice. Ultimately, we demonstrate that IL-36γ is a key regulator of neutrophil recruitment in the vaginal microenvironment and may function to limit HSV-2 neuroinvasion.
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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.
Texte intégralRésumé :
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, and assessed behavioral changes. C57Bl6 adult mice were maintained in an impoverished environment (IE) or enriched environment (EE) for four months and then subjected to the open field test. Afterwards, an equal volume of normal or virus-infected brain homogenate was nasally instilled. The brains were processed to detect viral antigens and microglial morphological changes using selective immunolabeling. We demonstrated earlier significant weight loss and higher mortality in IE mice. Additionally, behavioral analysis revealed a significant influence of the environment on locomotor and exploratory activity that was associated with less neuroinvasion and a reduced microglial response. Thus, environmental enrichment was associated with a more effective immune response in a mouse model of limbic encephalitis, allowing faster viral clearance/decreased viral dissemination, reduced disease progression, and less CNS damage.
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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.
Texte intégralRésumé :
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 71.7% of CSF and 22.7% of serum samples (p = 0.003). Expression of IL-2/IL-4/TNF-α and Th1 17 cytokines (IL-17A/IL-17F/IL-21) was detected in the serum but not in the CSF (except one positive CSF sample for IL-17F/IL-4). While IL-6 levels were markedly higher in the CSF compared to serum (CSF median 2036.71, IQR 213.82–6190.50; serum median 24.48, IQR 11.93–49.81; p < 0.001), no difference in the IL-13/IL-9/IL-10/IFN-γ/IL-22 levels in serum/CSF was found. In conclusion, increased concentrations of the key cytokines associated with innate and early acute phase responses (IL-6) and Th1 type immune responses (IFN-γ) were found in the CNS of patients with WNV infection. In contrast, expression of the key T-cell growth factor IL-2, Th17 cytokines, a Th2 cytokine IL-4 and the proinflammatory cytokine TNF-α appear to be concentrated mainly in the periphery.
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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.
Texte intégralRésumé :
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 manifestations and complications of COVID-19 are diverse: (1) cerebral circulatory disorders, including ischemic stroke and macro/microhemorrhages; (2) encephalopathy; (3) para/postinfectious autoimmune complications, such as GuillainBarre syndrome; (4) meningoencephalitis; (5) neuropsychiatric complications (psychosis and mood disorders). In terms of pathogenesis, neurological disorders in COVID-19 can be caused by neurotropicity and neurovirulence of SARS-CoV-2, cytokine storm, hypoxemia, homeostasis disorders, as well as their combined effects. COVID-19 adversely affects the course and prognosis of chronic neurological disorders in comorbid patients. The review highlights the need for vigilance to early neurological complications in patients infected with SARS-CoV-2 and other coronaviruses, especially since some neurological complications may precede respiratory manifestations.
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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.
Texte intégralRésumé :
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 phenotype. Remarkably, deletion of Irf5 alone resulted in meningoencephalitis and death on a more protracted timeline, 1 to 2 weeks after initial OROV or LACV infection. The clinical signs in OROV-infected Irf5 −/− mice were associated with abundant viral antigen and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells in several regions of the brain. Circulating dendritic cell (DC) subsets in Irf5 −/− mice had higher levels of OROV RNA in vivo yet produced lower levels of type I IFN than wild-type (WT) cells. This result was supported by data obtained in vitro , since a deficiency of IRF-5 resulted in enhanced OROV infection and diminished type I IFN production in bone marrow-derived DCs. Collectively, these results indicate a key role for IRF-5 in modulating the host antiviral response in peripheral organs that controls bunyavirus neuroinvasion in mice. IMPORTANCE Oropouche virus (OROV) and La Crosse virus (LACV) are orthobunyaviruses that are transmitted by insects and cause meningitis and encephalitis in subsets of individuals in the Americas. Recently, we demonstrated that components of the type I interferon (IFN) induction pathway, particularly the regulatory transcription factors IRF-3 and IRF-7, have key protective roles during OROV infection. However, the lethality in Irf3 −/− Irf7 −/− (DKO) mice infected with OROV was not as rapid or complete as observed in Ifnar −/− mice, indicating that other transcriptional factors associated with an IFN response contribute to antiviral immunity against OROV. Here, we evaluated bunyavirus replication, tissue tropism, and cytokine production in primary cells and mice lacking IRF-5. We demonstrate an important role for IRF-5 in preventing neuroinvasion and the ensuing encephalitis caused by OROV and LACV.
Thèses sur le sujet "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.
Texte intégralRésumé :
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, including the female reproductive tract (FRT) and may be an important factor in host defense. Although IL-36gamma has been shown to be induced in the FRT after exposure to microbial products, the contributions of IL-36gamma to host defense mechanisms in response to this clinically relevant STI pathogen are not well understood. This dissertation describes the regulation of IL-36gamma in the FRT and explores its contribution to the host response against genital HSV-2 infection.
To test the hypothesis that IL-36gamma is a key regulator of mucosal inflammation and immunity in the FRT, hormonal regulation of IL-36gamma in the FRT was investigated using estrogen- and progesterone-conditioned mice. From this preliminary study, it was shown that progesterone dampens IL36G expression relative to estrogen and may potentially increase susceptibility to infection. Next, the impact of IL-36gamma treatment on HSV-2 infection and replication in human 3-D vaginal epithelial cells was explored. In parallel, the impact of intravaginal IL-36gamma delivery on HSV-2 disease pathogenesis was evaluated using a lethal murine challenge model. IL-36gamma pre-treatment significantly limited HSV-2 replication in vitro and in vivo and was associated with transient neutrophil infiltration that corresponded with decreased disease severity and increased survival in mice. Last, the requirement for IL-36gamma in host defense was investigated utilizing IL-36gamma-/- mice in a lethal HSV-2 murine challenge model. Following infection, IL-36gamma-/- mice exhibited significantly impaired neutrophil recruitment, decreased overall survival time, and significantly increased viral neuroinvasion relative to wild type mice. Collectively, these data indicate that IL-36gamma is a crucial regulator of HSV-2-induced neutrophil infiltration and appears to function in a previously uncharacterized manner to limit viral neuroinvasion in genital HSV-2 disease pathogenesis.<br>Dissertation/Thesis<br>Doctoral Dissertation Molecular and Cellular Biology 2019
Chapitres de livres sur le sujet "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.
Texte intégralRésumé :
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 (IL)-6, IL-17, IL-1b, and tumor necrosis factor (TNF), is able to disrupt the BBB. The neuroinvasive nature of SARS-CoV-2 has a more severe impact on patients with preexisting neurological manifestations such as Parkinson’s disease (PD). Pathological features of PD include selective loss of dopaminergic neurons in the substantia nigra pars compacta and aggregation of α-syn proteins present in neurons. Interaction between SARS-COV-2 infection and α-synuclein might have long-term implications on the onset of Parkinsonism by the formation of toxic protein clumps called amyloid fibrils—a hallmark of Parkinson’s. Molecular modeling is an emerging tool to predict potential inhibitors against the enzyme α-synuclein in neurodegenerative diseases by using plant bioactive molecules.
Actes de conférences sur le sujet "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.
Texte intégralRésumé :
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 connection, or not, between neurological manifestations and SARS-CoV-2 infection. Design and setting: Analysis of the current literature present in medical databases. Methods: To select the studies, the Medline (Pubmed), LILACS and SciELO databases were used with the keywords “neurology” and “covid” and “mechanism”. The search period for the articles covered the last 10 months (since June 2020). The selection and design criteria of the studies were descriptive, crosssectional, cohort, case report and randomized clinical study. Results: Thirty-eight articles with potential for inclusion were retrieved, but only seventeen of them declared no conflict of interest and answered the inclusion criteria and the guiding question, which consisted of assessing the association between neurological disorders and COVID-19. Conclusion: Eight studies defend the indirect invasion, due to the imaging exams presenting an olfactory bulb without any alteration. Through infection of the endothelial cells, vascular alterations and wear of the BBB by the cytokine storm. In parallel, the other nine studies advocate direct invasion, where the virus infects the olfactory bulb and reaches the rhinencephalon and midbrain through the axons, generating, for example, the lack of symptoms in the so-called happy hypoxia of the coronavirus. Neuroinvasion in COVID-19 is still unclear, but hypotheses show 2 possible pathways for the virus to access the CNS: hematogenous and retrograde neuronal pathways. To elucidate these pathogenic pathways, larger and more systematic studies will be needed.