Stockholm University and Karolinska Institutet have discovered that viruses can bind a special class of proteins called amyloid proteins that play a part in cell death and can lead to Alzheimer’s disease.
New research from Stockholm University and Karolinska Institutet shows that viruses interact with proteins in the biological fluids of their host which results in a layer of proteins on the viral surface. This coat of proteins makes the virus more infectious and facilitates the formation of plaques (created from amyloid proteins) characteristic of neurodegenerative diseases such as Alzheimer’s disease.
What do you know about viruses?
Viruses can only reproduce inside living cells and exploit the cellular machinery of their host to their benefit. However, before entering a host cell, viruses are just nanometre-sized particles, very similar to artificial nanoparticles used in medical applications such as diagnosis and therapy.
Scientists from the respective institutes have found that viruses and nanoparticles share another important property; they both become covered by a layer of proteins when they encounter the biological fluids of their host before they find their target cell. This layer of proteins on the surface influence their biological activity significantly.
Kariem Ezzat of Stockholm University and Karolinska Institutet, explains: “Imagine a tennis ball falling into a bowl of milk and cereals. The ball is immediately covered by the sticky particles in the mix and they remain on the ball when you take it out of the bowl. The same thing happens when a virus gets in contact with blood or lung fluids that contain thousands of proteins. Many of these proteins immediately stick to the viral surface forming a so-called protein corona.”
Binding the special class of proteins: amyloid proteins
The researchers found that viruses such as RSV and herpes simplex virus type 1 (HSV-1) can bind a special class of proteins called amyloid proteins. Amyloid proteins aggregate into plaques that play a part in Alzheimer’s disease where they lead to neuronal cell death.
The mechanism behind the connection between viruses and amyloid plaques has been hard to find till now, but Ezzat and his colleagues found that HSV-1 is able to accelerate the transformation of soluble amyloid proteins into thread-like structures that constitute the amyloid plaques. In animal models of Alzheimer’s disease, they saw that mice developed the disease within 48 hours of infection in the brain. In absence of an HSV-1 infection the process normally takes several months.
“The novel mechanisms described in our paper can have an impact not only on understanding new factors determining how infectious a virus is, but also on devising new ways to design vaccines.
“In addition, describing a physical mechanism that links viral and amyloid causes of disease adds weight to the increasing research interest in the role of microbes in neurodegenerative disorders such as Alzheimer’s disease and opens up new avenues for treatments.” Ezzat concludes.
