Viral amyloids: New opportunities for antiviral therapeutic strategies
Frank Gondelaud, Pierre‐Yves Lozach, Sonia Longhi
Abstract
Amyloidoses are an array of diseases associated with the aggregation of proteins into fibrils. While it was previously thought that amyloid fibril-forming proteins are exclusively host-cell encoded, recent studies have revealed that pathogenic viruses can form amyloid-like fibrils too. Intriguingly, viral amyloids are often composed of virulence factors, known for their contribution to cell death and disease progression. In this review, we survey the literature about viral proteins capable of forming amyloid-like fibrils. The molecular and cellular mechanisms underlying the formation of viral amyloid-like aggregates are explored. In addition, we discuss the functional implications for viral amplification and the complex interplay between viral amyloids, biological functions, virulence, and virus-induced pathologies. • Numerous viruses code for amyloid-like fibril-forming proteins. • Several viral amyloids have functional significance that can benefit viruses. • Interactomics of viral amyloid-forming proteins revealed few shared host partners. • Viral amyloids are potentially linked to neurodegeneration. • Targeting viral amyloids represents a promising antiviral strategy.