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Image source: Stockholm University
Recently, new research from Stockholm University in Sweden and Karolinska School of Medicine shows that viruses interact with proteins in host organisms, thus forming a protein "coat" on the surface of the virus, which makes the virus more infectious and promotes the formation of neurodegenerative diseases, such as the formation of characteristic plaques in Alzheimer's disease. The study has been published recently in Nature Communications.
Is the virus dead or alive? Well, both statements are correct. Viruses can only reproduce in living cells and use the host's cellular mechanism to benefit themselves. However, before entering the host cell, the virus is just nano-sized particles, very similar to the artificial nanoparticle used for medical diagnosis and treatment. The research team found that viruses and nanoparticles have another important property: when they encounter the host's biological fluid before finding the target cell, they are covered with a layer of protein, which greatly affects their biological activity. "Imagine a tennis ball falls into a bowl of milk cereal, and the tennis ball is immediately covered with sticky particles, and when the balls are removed from the bowl, they remain on the balls. The same happens when the virus comes into contact with blood or lung fluid containing thousands of proteins."
Ezzat and colleagues studied the protein crown of respiratory syncytial virus (RSV) in different biological fluids. RSV is the most common cause of acute lower respiratory tract infection in children around the world, causing 34 million cases and 196,000 deaths each year.
Image source: "Nature Communications"
Ezzat said: "The protein corona characteristics of RSV in the blood are very different from those in the lung fluid. There are also differences between humans and other species, such as rhesus monkeys, which may also be infected with RSV. This virus remains unchanged at the genetic level, and it accumulates different 'protein crowns' on its own surface area only according to the environment, thereby obtaining different identities. This makes it possible for the virus to use extracellular host factors to benefit itself. We have shown that many different protein crowns make RSV more contagious." The research team also found that viruses such as RSV and herpes simplex virus type 1 (HSV-1) can bind to a special class of amyloid proteins, which accumulate into plaques, play a role in Alzheimer's disease and lead to nerve cell death. It is still difficult to find the mechanism of the link between viruses and amyloid plaques. But Ezzat and colleagues found that HSV-1 could accelerate the transition of soluble amyloid proteins to filamentous structures that make up amyloid plaques. In an animal model of Alzheimer's disease, they found that mice develop within 48 hours of brain infection, and the process usually takes several months without HSV-1 infection.
Image Source: "Nature Communications"
Ezzat said: "The new mechanisms we describe in the paper can not only affect understanding the new factors that determine the infectivity of the virus, but also help design new vaccines. In addition, describing a physical mechanism that links the pathogenic causes of viruses and amyloids can increase scholars' research interest in the role of microorganisms in neurodegenerative diseases such as Alzheimer's disease, and open up new avenues for treatment."
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