West Nile Virus-Induced Neurologic Sequelae—Relationship to Neurodegenerative Cascades and Dementias

Vittor, Amy Y.; Long, Maureen T.; Chakrabarty, Paramita; Aycock, Lauren; Kollu, Vidya; DeKosky, Steven T.

doi:10.1007/s40475-020-00200-7

Cited by 16 publications

(14 citation statements)

References 152 publications

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“…In humans, Lewy body formation is linked to the development of Parkinson's disease or Lewy body dementia (22,23). It has been hypothesized that certain neurotropic viruses, including MERS and SARS coronaviruses, can trigger formation of Lewy bodies and cause Parkinsonism (24)(25)(26)(27)(28)(29).…”

mentioning

confidence: 99%

SARS-CoV-2 causes brain inflammation and induces Lewy body formation in macaques

Philippens

Böszörményi

Wubben

et al. 2021

Preprint

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SARS-CoV-2 may cause acute respiratory disease, but the infection can also initiate neurological symptoms. Here we show that SARS-CoV-2 infection causes brain inflammation in the macaque model. An increased metabolic activity in the pituitary gland of two macaques was observed by longitudinal positron emission tomography-computed tomography (PET-CT). Post-mortem analysis demonstrated infiltration of T-cells and activated microglia in the brain, and viral RNA was detected in brain tissues from one animal. We observed Lewy bodies in brains of all rhesus macaques. These data emphasize the virus' capability to induce neuropathology in this nonhuman primate model for SARS-CoV-2 infection. As in humans Lewy body formation is an indication for the development of Parkinson's disease, this data represents a warning for potential long-term neurological effects after SARS-CoV-2 infection.

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confidence: 99%

SARS-CoV-2 causes brain inflammation and induces Lewy body formation in macaques

Philippens

Böszörményi

Wubben

et al. 2021

Preprint

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“…6 The link between WNV infections and neurodegenerative diseases has been reviewed recently. 7 WNV accesses the CNS either by endothelial passive transport, by using leukocytes as a "Trojan horse," by retrograde axonal transport after infection of peripheral nerves, or by leaking into tight junctions that are weakened by tumor necrosis factor-α-induced peripheral inflammation. In the latter case, arterial hypertension, as was present in our patient, can help weakening the blood-brain barrier.…”

Section: Discussionmentioning

confidence: 99%

West Nile Virus Neuroinvasive Disease Accelerating Probable Dementia With Lewy Bodies

Segers

Ranst

Bostan

et al. 2020

Alzheimer Disease &Amp; Associated Disorders

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We describe a case of dementia with Lewy bodies immediately following encephalitis due to West Nile virus (WNV). The patient had rapid eye movement-sleep behavior disorder and constipation before the onset of encephalitis, which suggests that he would have ultimately developed dementia with Lewy bodies even without WNV infection. Our case illustrates the interactions between α-synuclein and WNV, as observed in mouse models, wherein synuclein expression augments after WNV infection and protects neurons against the virus.

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“…The pathological features of these patients overlap with those of Alzheimer's disease (AD) and Parkinson's disease (PD) and are presumably caused by direct neural damage and long-term production of proinflammatory cytokines (e.g., IFN-γ, TNFα, Il-1β) secreted by WNV specific T cells [117,118]. In mice, WNV RNA was found up to 6 months post infection [72]. Other members of the Flavivirus family were also reported to cause PAS [73,74].…”

Section: (+) Ssrna Virusesmentioning

confidence: 99%

Implications of Innate Immunity in Post-Acute Sequelae of Non-Persistent Viral Infections

Hirschenberger

Hunszinger

Sparrer

2021

Cells

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Non-persistent viruses classically cause transient, acute infections triggering immune responses aimed at the elimination of the pathogen. Successful viruses evolved strategies to manipulate and evade these anti-viral defenses. Symptoms during the acute phase are often linked to dysregulated immune responses that disappear once the patient recovers. In some patients, however, symptoms persist or new symptoms emerge beyond the acute phase. Conditions resulting from previous transient infection are termed post-acute sequelae (PAS) and were reported for a wide range of non-persistent viruses such as rota-, influenza- or polioviruses. Here we provide an overview of non-persistent viral pathogens reported to be associated with diverse PAS, among them chronic fatigue, auto-immune disorders, or neurological complications and highlight known mechanistic details. Recently, the emergence of post-acute sequelae of COVID-19 (PASC) or long COVID highlighted the impact of PAS. Notably, PAS of non-persistent infections often resemble symptoms of persistent viral infections, defined by chronic inflammation. Inflammation maintained after the acute phase may be a key driver of PAS of non-persistent viruses. Therefore, we explore current insights into aberrant activation of innate immune signaling pathways in the post-acute phase of non-persistent viruses. Finally, conclusions are drawn and future perspectives for treatment and prevention of PAS are discussed.

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West Nile Virus-Induced Neurologic Sequelae—Relationship to Neurodegenerative Cascades and Dementias

Cited by 16 publications

References 152 publications

SARS-CoV-2 causes brain inflammation and induces Lewy body formation in macaques

SARS-CoV-2 causes brain inflammation and induces Lewy body formation in macaques

West Nile Virus Neuroinvasive Disease Accelerating Probable Dementia With Lewy Bodies

Implications of Innate Immunity in Post-Acute Sequelae of Non-Persistent Viral Infections

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