Fig. 1: mechanisms leading to neurodegenerative diseases after virus infection. Virus infection can collectively trigger different alterations in cell processes through three main mechanisms: 1. It alters protein metabolism, perturbing protein synthesis and degradation (protein ubiquitination, degradation at the proteasome, and autophagy/aggrephagy). It also affects chaperon prevention/correction of protein misfolding. 2. Viruses can directly interact with proteins, leading to structural conversion, starting aggregation, and forming small toxic aggregates and amyloid fibrils. These fibrils can seed monomer aggregation, representing a self-replicating process. Different virus molecules, such as proteins, lipids, and nucleic acids, are supposed to show this property. 3. Viruses perturb post-translational protein modifications, modulating protein function and oligomerisation. For example, Tau hyperphosphorylation, associated with Alzheimer’s disease, can be triggered by a virus infection, leading to the formation of neurofibrillary tangles and cell dysfunction. This figure was designed at Biorender.com.
