Protein coatings contain more viruses and connect them to Alzheimer's disease

Protein coatings contain more viruses and connect them to Alzheimer's disease

New research from the University of Stockholm and Karolinska Institutet shows that viruses interact with proteins in the biological fluids of their host which result in a series of proteins on the viral surface. This proteins coat makes the virus more infectious and facilitates the formation of plaque characteristics of neurodegenerative diseases such as Alzheimer's disease.

Are viruses dead or alive? Well … both. Viruses can only be reproduced within live cells and benefit from cellular machinery to host their advantage. However, before entering a host cell, a single nanometer size is a particle of viruses, which is very similar to artificial nanoparticles used in medical applications for diagnosis and therapy. Scientists from the University of Stockholm and Karolinska Institutet found that viruses and nanoparticles divide another important property; they are both covered by a series of proteins when they come to the biological fluids of their hotels before they reach their target cell. This series significantly affects proteins on the surface of their biological activity.

"Imagine having a tennis ball falling into a bowl of milk and cereal. The sticky particles cover the ball immediately and stay on the ball when you take it out of the bowl. The same thing happens when a virus comes into contact with fluids. blood or lung containing thousands of proteins. Many of these proteins are immediately adhering to the viral surface that creates a so-called protein coronary ”, explains Kariem Ezzat from the University of Stockholm and Karolinska Institutet.

Kariem Ezzat and his colleagues studied the protein crown of the synchronous respiratory virus (RSV) in various biological fluids. RSV is the most common cause of lower respiratory tract infections in young children worldwide, leading to up to 34 million cases and 196,000 deaths each year. "The coronary protein signature on RSV in the blood is very different from that in lung fluid. It is also different from other people and species such as rowan macaque monkeys, which can also be infected with RSV", said Kariem Ezzat. "The virus remains unchanged at the genetic level. It is only possible to find different identities by accumulating different protein crowns on its surface depending on its surroundings. This allows the virus to use exclusive host factors for its benefit. and we showed that many of these different coronae make RSV more infectious. "

The researchers from the University of Stockholm and Karolinska Institutet also found that viruses such as RSV virus and herpes 1 (HSV-1) can require a special class of proteins called amyloid proteins. Plaques taking part in Alzheimer's disease have aggregated Amyloid proteins where they result in neuronal cell death. The mechanism behind the link between viruses and amyloid plaques has been difficult to find so far, but Kariem Ezzat and his colleagues found that HSV-1 is capable of accelerating the transformation of soluble amyloid proteins into structures such as thread. 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 the absence of HSV-1 infection the process usually takes several months.

"The novel mechanisms described in our paper can have an impact, not only on understanding new factors that determine how infectious a virus is, but also in designing new ways to design vaccines." , describes a physical mechanism that links viral and amyloid causes of diseases that contribute to the increased interest in research in the role of microbes in neurodegenerative disorders such as Alzheimer's disease and opens new ways of treatment. ", says Kariem Ezzat from Stockholm University and Karolinska Institutet .

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"The Viral Protein Corona Pathogenesis and Amyloid Aggreg" are published by Ezzat et al i Nature Communications. DOI: 10.1038 / s41467-019-10192-2. The project is a collaboration between a researcher from the University of Stockholm, Karolinska Institutet and the University of Eastern Finland and others.

more information

Kariem Ezzat, Department of Molecular Sciences, Wenner-Gren Institute, Stockholm University and Department of Medical Laboratory, Karolinska Institutet. Phone: + 46 8 16 14 37, mobile: +46 720 39 09 93, email: kariem.ezzat@su.se

Anna-Lena Spetz, Department of Molecular Sciences, Wenner-Gren Institute, Stockholm University. Phone: +46 8 16 42 05, Mobile +46 707 47 13 03, e-mail: anna-lena.spetz@su.se

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