Researchers recently discovered when a layer of protein develops on the viral surface it can make the virus more infectious and form plaques, which is associated with Alzheimer’s disease. The interaction takes place due to the host's biological fluids.
The study was conducted by a team fromStockholm University and Karolinska Institutet. "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. Many of these proteins immediately stick to the viral surface forming a so-called protein corona,” study author Kariem Ezzat of Stockholm University and Karolinska Institutet told a news portal.
The team examined the protein corona of respiratory syncytial virus (RSV) in various biological fluids. RSV is a major cause of acute lower respiratory tract infections in children across the globe. Annually, this disease gives rise to close to 34 million cases and 196,000 fatalities. "The protein corona signature of RSV in the blood is very different from that in lung fluids. It is also different between humans and other species such as rhesus macaque monkeys, which also can be infected with RSV," Ezzat told a news portal. Adding, "The virus remains unchanged on the genetic level. It just acquires different identities by accumulating different protein coronae on its surface depending on its environment. This makes it possible for the virus to use extracellular host factors for its benefit, and we have shown that many of these different coronae make RSV more infectious."
The team also discovered that viruses similar to RSV and herpes simplex virus type 1 (HSV-1) can tie together proteins called amyloid proteins, which transform into plaques. This can increase the risk of Alzheimer’s disease as it leads to the death of neuronal cells.
The findings have brought scientists a step closer to understanding the association between viruses and amyloid plaques. Ezzat and his team revealed HSV-1 can turn amyloid proteins into plaques at a rapid pace. "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," Ezzat told a news portal. Adding, "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."
The study's findings were originally published in the journal Nature Communications.
