阿尔兹海默症 z-bo 2020-10-26 356

　　The latest research by Stockholm University and Karolinska Institutet shows that viruses interact with proteins in host biological fluids to form a layer of protein on the surface of the virus. This protein coat makes the virus more contagious and promotes the formation of plaques in neurodegenerative diseases such as Alzheimer's disease.

　　Is the virus dead or alive? Um...both. Viruses can only reproduce in living cells and use the host's cellular machinery to provide nutrition for themselves. However, before entering host cells, viruses are just nano-sized particles, very similar to artificial nanoparticles used in medical diagnosis and treatment. Scientists at Stockholm University and Karolinska Institutet have discovered that viruses and nanoparticles have another important property: When they encounter the host’s biological fluid before finding the target cell, they will be Cover with a layer of protein. This layer of protein on the surface has a significant effect on their biological activity.

　　Imagine a tennis ball falling into a bowl of milk and cereal. When you take the ball out of the bowl, the ball is immediately covered by the sticky particles in the mixture. The same happens when the virus comes into contact with blood or lung fluid containing thousands of proteins.

　　Kariem Ezzat and his colleagues studied the respiratory syncytial virus (RSV) protein corona in different biological fluids. RSV is the most common cause of acute lower respiratory tract infections in children worldwide, causing 34 million cases and 196,000 deaths each year. "RSV has a very different protein crown in the blood and lung fluid. It is also different between humans and other species, such as rhesus monkeys, which can also be infected with RSV," Ezzat said. "The virus remains the same at the genetic level. It just accumulates different protein canopies on the surface to obtain different identities, depending on the environment it is in. This makes it possible for the virus to use extracellular host factors to gain benefits. We have shown that many different coronary bodies make RSV more contagious."

　　Researchers at Stockholm University and Karolinska Institute also discovered that viruses such as RSV and herpes simplex virus type 1 (HSV-1) can bind to a special type of protein called amyloid. Amyloid aggregates into plaques and plays a role in Alzheimer's disease, causing neuronal cell death. So far, the mechanism of the connection between the virus and amyloid plaques is still difficult to find, but Ezzat and his colleagues found that HSV-1 can accelerate the transformation of soluble amyloid into the linear structure that constitutes amyloid plaques. In an animal model of Alzheimer's disease, they found that mice developed the disease within 48 hours of a brain infection. In the absence of HSV-1 infection, this process usually takes several months.

　　"The new mechanism described in our paper can affect not only the understanding of new factors that determine the infectivity of viruses, but also new methods for designing vaccines. In addition, we describe a link between viruses and amyloid. This will increase our interest in research on the role of microorganisms in neurodegenerative diseases such as Alzheimer’s disease and open up new approaches for treatment."