Viruses and amyloids - a vicious liaison

Area of Science:

• Neurovirology
• Molecular Biology
• Protein Chemistry

Background:

• The interplay between viral infections, amyloidogenesis, and neurodegenerative diseases has been recognized for decades.
• Several viruses harbor amyloidogenic proteins, and viral infections can trigger post-acute sequelae (PAS).
• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease 2019 (COVID-19) highlight potential links between amyloid formation and disease severity, PAS, and neurodegeneration.

Approach:

• This review examines the convergence of viral and amyloid research.
• It explores evolutionary pressures on protein amyloid formation in viruses versus other organisms.
• The review discusses common mechanisms like posttranslational endoproteolysis in amyloid formation for viral and human proteins.

Key Points:

• Viral and human proteins can form amyloids independently and cooperatively, influencing inter- and intra-host spread.
• Abnormal blood clotting in severe/long COVID and vaccine side effects are linked to fibrin and Spike protein amyloid formation.
• Amyloid formation propensity differs between viruses and host organisms due to distinct evolutionary drivers.

Conclusions:

• There are significant overlaps between viral and amyloid research, necessitating collaborative efforts.
• Accelerating antiviral drug development is crucial to prevent PAS and neurological damage.
• Developing next-generation vaccines requires revisiting suitable antigen targets for pandemic preparedness.