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Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Epublish 17 citations

PubMed: 36139092 DOI: 10.3390/biom12091253

SARS-CoV-2 Invasion and Pathological Links to Prion Disease.

Biomolecules 12(9)

Authors: Walter J Lukiw, Vivian R Jaber, Aileen I Pogue, Yuhai Zhao

Affiliations

  • LSU Neuroscience Center, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.
  • Alchem Biotek Research, Toronto, ON M5S 1A8, Canada.
  • Department of Ophthalmology, LSU Health Science Center, New Orleans, LA 70112, USA.
  • Department Neurology, LSU Health Science Center, New Orleans, LA 70112, USA.
  • LSU Neuroscience Center, Louisiana State University Health Science Center, New Orleans, LA 70112, USA. Department of Cell Biology & Anatomy, LSU Health Science Center, New Orleans, LA 70112, USA.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the COVID-19 disease, is a highly infectious and transmissible viral pathogen that continues to impact human health globally. Nearly ~600 million people have been infected with SARS-CoV-2, and about half exhibit some degree of continuing health complication, generically referred to as long COVID. Lingering and often serious neurological problems for patients in the post-COVID-19 recovery period include brain fog, behavioral changes, confusion, delirium, deficits in intellect, cognition and memory issues, loss of balance and coordination, problems with vision, visual processing and hallucinations, encephalopathy, encephalitis, neurovascular or cerebrovascular insufficiency, and/or impaired consciousness. Depending upon the patient’s age at the onset of COVID-19 and other factors, up to ~35% of all elderly COVID-19 patients develop a mild-to-severe encephalopathy due to complications arising from a SARS-CoV-2-induced cytokine storm and a surge in cytokine-mediated pro-inflammatory and immune signaling. In fact, this cytokine storm syndrome: (i) appears to predispose aged COVID-19 patients to the development of other neurological complications, especially those who have experienced a more serious grade of COVID-19 infection; (ii) lies along highly interactive and pathological pathways involving SARS-CoV-2 infection that promotes the parallel development and/or intensification of progressive and often lethal neurological conditions, and (iii) is strongly associated with the symptomology, onset, and development of human prion disease (PrD) and other insidious and incurable neurological syndromes. This commentary paper will evaluate some recent peer-reviewed studies in this intriguing area of human SARS-CoV-2-associated neuropathology and will assess how chronic, viral-mediated changes to the brain and CNS contribute to cognitive decline in PrD and other progressive, age-related neurodegenerative disorders.

MeSH

Infections, Aged, Prion Diseases, Brain, Prions, Sars Virus, Cytokine Release Syndrome, Covid-19, Sars-Cov-2

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