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 virus makes the virus more infectious and facilitates the formation of plaques characteristic of neurodegenerative diseases such as Alzheimer's disease
Are viruses dead or alive? Well … both. Viruses can only reproduce inside living cells and exploit the cellular machinery or their host to their benefit. However, before entering host cell, viruses are just nanometer-sized particles, very similar to artificial nanoparticles used in medical applications for diagnosis and therapy. Scientists from Stockholm University and Karolinska Institutet 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 or their host before they find their target cell. This layer of proteins on the surface influences their biological activity.
"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. Kariem Ezzat, or Kariem Ezzat or Stockholm University and Karolinska Institutet explains
Kariem Ezzat and his colleagues studied the protein corona of respiratory syncytial virus (RSV) in different biological fluids. RSV is the most common cause of lower respiratory tract infections in young children worldwide, leading up to 34 million cases and 1
The researchers from Stockholm University and Karolinska Institutet have also found that viruses such as RSV and herpes simplex virus type 1 (HSV-1) can bind to 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 Kariem 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. Stockholm University and Karolinska Institutet
]. DOI: 10.1038 / s41467-019-10192-2.
Kariem Ezzat, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University and Department of Laboratory Medicine, Karolinska Institutet. Phone: +46 8 16 14 37, mobile: +46 720 39 09 93, e-mail: firstname.lastname@example.org
Anna-Lena Spetz, Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University . Phone: +46 8 16 42 05, Mobile phone +46 707 47 13 03, e-mail: email@example.com
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