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The University of Stockholm and the Karolinska Institutet have discovered that viruses can bind to a special clbad of proteins called amyloid proteins, which play a role in cell death and can lead to Alzheimer's disease.
A new study from the Stockholm University and Karolinska Institutet shows that viruses interact with the proteins contained in the biological fluids of their host, resulting in the formation of a layer of protein on the surface of the virus . This layer of protein makes the virus more infectious and facilitates the formation of plaques (made 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 make the best use of the cellular mechanisms of their host. However, before entering a host cell, viruses are only nanoscale particles, very similar to artificial nanoparticles used in medical applications such as diagnosis and therapy.
Scientists at the respective institutes have discovered that viruses and nanoparticles share another important property. they both overlap with a layer of proteins when they encounter the biological fluids of their host before finding their target cell. This layer of proteins on the surface considerably influences their biological activity.
Kariem Ezzat, of Stockholm University, and the Karolinska Institutet, explain: "Imagine a tennis ball that falls into a bowl of milk and cereals. The ball is immediately covered by the sticky particles of the mixture and these remain on the ball when you take it out of the bowl. The same thing happens when a virus comes in contact with blood or lung fluids containing thousands of proteins. Many of these proteins immediately adhere to the viral surface, forming a protein called a crown. "
Liaison of the special clbad of proteins: amyloid proteins
The researchers found that viruses such as RSV and herpes simplex virus type 1 (HSV-1) can bind to a special clbad of proteins called amyloid proteins. Amyloid proteins aggregate into plaques that play a role in Alzheimer's disease and cause death of neuronal cells.
The mechanism behind the link between viruses and amyloid plaques was hard to find until now, but Ezzat and his colleagues discovered that HSV-1 is able to accelerate the transformation of soluble amyloid proteins in filiform structures constituting amyloid plaques. In animal models of Alzheimer's disease, they found that mice developed the disease within 48 hours of brain infection. In the absence of HSV-1 infection, the process normally takes several months.
"The innovative mechanisms described in our paper can have an impact not only on understanding new factors determining the infectivity of a virus, but also on designing new vaccine design methods.
"In addition, the description of a physical mechanism that links the viral and amyloid causes of the disease adds weight to the growing interest of research in the role of microbes in neurodegenerative diseases such as Alzheimer's disease." Alzheimer's and opens new ways of treatment, "concludes Ezzat.
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