Neurological Damage by Coronaviruses: A Catastrophe in the Queue!

Mishra, Ritu; Banerjea, Akhil C.

doi:10.3389/fimmu.2020.565521

Cited by 48 publications

(47 citation statements)

References 139 publications

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“…CNS is potentially susceptible for this virus infection as reports clearly indicate COVID-19 patients suffering from neurological signs such as anosmia (loss of taste and smell), nausea, vomiting, headache and cerebral damages (stroke, encephalitis and degenerative symptoms) (13). Presence of SARS-CoV in brain tissues have also been reported before (14) and it is generally suggested that SARS-CoV-2 enters the brain by both route via hematogenous route as well as olfactory bulb through retrograde neuronal travel (10,15,16).…”

Section: Introductionmentioning

confidence: 90%

“…Neurological damages by coronaviruses are now an established observation, supported by many experimental and clinical reports (10)(11)(12). CNS is potentially susceptible for this virus infection as reports clearly indicate COVID-19 patients suffering from neurological signs such as anosmia (loss of taste and smell), nausea, vomiting, headache and cerebral damages (stroke, encephalitis and degenerative symptoms) (13).…”

Section: Introductionmentioning

confidence: 95%

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SARS-CoV-2 Spike Targets USP33-IRF9 Axis via Exosomal miR-148a to Activate Human Microglia

Mishra

Banerjea²

2021

Front. Immunol.

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SARS-CoV-2, the novel coronavirus infection has consistently shown an association with neurological anomalies in patients, in addition to its usual respiratory distress syndrome. Multi-organ dysfunctions including neurological sequelae during COVID-19 persist even after declining viral load. We propose that SARS-CoV-2 gene product, Spike, is able to modify the host exosomal cargo, which gets transported to distant uninfected tissues and organs and can initiate a catastrophic immune cascade within Central Nervous System (CNS). SARS-CoV-2 Spike transfected cells release a significant amount of exosomes loaded with microRNAs such as miR-148a and miR-590. microRNAs gets internalized by human microglia and suppress target gene expression of USP33 (Ubiquitin Specific peptidase 33) and downstream IRF9 levels. Cellular levels of USP33 regulate the turnover time of IRF9 via deubiquitylation. Our results also demonstrate that absorption of modified exosomes effectively regulate the major pro-inflammatory gene expression profile of TNFα, NF-κB and IFN-β. These results uncover a bystander pathway of SARS-CoV-2 mediated CNS damage through hyperactivation of human microglia. Our results also attempt to explain the extra-pulmonary dysfunctions observed in COVID-19 cases when active replication of virus is not supported. Since Spike gene and mRNAs have been extensively picked up for vaccine development; the knowledge of host immune response against spike gene and protein holds a great significance. Our study therefore provides novel and relevant insights regarding the impact of Spike gene on shuttling of host microRNAs via exosomes to trigger the neuroinflammation.

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Section: Introductionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 95%

SARS-CoV-2 Spike Targets USP33-IRF9 Axis via Exosomal miR-148a to Activate Human Microglia

Mishra

Banerjea²

2021

Front. Immunol.

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“…Immune cells infected with virus may attach to the brain endothelial cells and traverse across this layer and then come into contact with neurons. This may also occur with virus at the meningeal-cerebrospinal barrier and with virus present within blood vessels at the choroid plexus [13][14][15]. Infection with some neurotropic viruses has been reported to lead to encephalitis which can be fatal in some cases [6].…”

Section: Viral Infection Of the Cnsmentioning

confidence: 99%

Back to the future: lessons from past viral infections and the link with Parkinson’s disease

Dowd

McKernan

2021

Neuronal Signaling

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During the current COVID-19 pandemic, there has been noticeable increase in the reporting of neurological symptoms in patients. There is still uncertainty around the significance and long-term consequence of these symptoms. There are also many outstanding questions on whether the causative virus SARS-CoV2 can directly infect the central nervous system. Given the long association between viral infections with neurodegenerative conditions such as Parkinson’s disease, it seems timely to review this literature again in the context of the COVID-19 pandemic and to glean some useful information from studies on similar viruses. In this commentary, we will consider the current knowledge on viral infections in the brain. In addition, we review the link between viral infection and neurodegeneration in Parkinson’s disease, and review the recent literature on SARS infections, the potential link with Parkinson’s disease and the potential areas of study in the future

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“…However, it is still debated whether or not the virus directly infects the CNS. One study in this area of research did not report evidence of the presence of SARS-CoV-2 or its particles in the brain during the autopsy of patients with COVID-19, in spite of the viral invasion in various organs However, a first study did not report evidence of the presence of SARS-CoV-2 or its particles in the brain at autopsy of patients with COVID-19 infection in spite of the invasion of the virus in various organs such as lungs, liver and heart [ 47 ]. On the other hand, Moriguchi et al [ 48 ] observed viral RNA in the cerebrospinal fluid of a patient with aseptic encephalitis and Paniz-Mandolfi et al [ 49 ] reported the presence of SARS-CoV-2 viral particles in the neuronal and capillary endothelial cells in the frontal lobe tissue in a postmortem study.…”

Section: Pathogenesis Of Neuro-covidmentioning

confidence: 99%

Emerging Neurological and Psychobiological Aspects of COVID-19 Infection

et al. 2020

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The SARS-CoV-2 virus, first reported in December 2019 in China, is the causative agent of the current COVID-19 pandemic that, at the time of writing (1 November 2020) has infected almost 43 million people and caused the death of more than 1 million people. The spectrum of clinical manifestations observed during COVID-19 infection varies from asymptomatic to critical life-threatening clinical conditions. Emerging evidence shows that COVID-19 affects far more organs than just the respiratory system, including the heart, kidneys, blood vessels, liver, as well as the central nervous system (CNS) and the peripheral nervous system (PNS). It is also becoming clear that the neurological and psychological disturbances that occur during the acute phase of the infection may persist well beyond the recovery. The aim of this review is to propel further this emerging and relevant field of research related to the pathophysiology of neurological manifestation of COVID-19 infection (Neuro-COVID). We will summarize the PNS and CNS symptoms experienced by people with COVID-19 both during infection and in the recovery phase. Diagnostic and pharmacological findings in this field of study are strongly warranted to address the neurological and psychological symptoms of COVID-19.

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Neurological Damage by Coronaviruses: A Catastrophe in the Queue!

Cited by 48 publications

References 139 publications

SARS-CoV-2 Spike Targets USP33-IRF9 Axis via Exosomal miR-148a to Activate Human Microglia

SARS-CoV-2 Spike Targets USP33-IRF9 Axis via Exosomal miR-148a to Activate Human Microglia

Back to the future: lessons from past viral infections and the link with Parkinson’s disease

Emerging Neurological and Psychobiological Aspects of COVID-19 Infection

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