A Common Virus May Play Role in Alzheimer’s disease, Study Finds

It has long been a controversial theory about Alzheimer’s disease, often dismissed by experts as a sketchy cul-de-sac off the beaten path from mainstream research.

Virus 'identity change' may play a task in Alzheimer's?

According to recent research in vitro and in mice, viruses that inherit contact with biological fluids acquire a protein coating that renders them more infectious.

Moreover, it seems that some viruses that ‘change identity’ in this way may promote neurodegenerative conditions, like Alzheimer’s.

Viruses are strange, fascinating agents, not least because scientists still find it difficult to mention whether or not they qualify as living organisms or not.

To replicate, viruses need to infect a number — so during a live biological environment, viruses are also “alive,” interacting with the cells of the host they infect and multiplying.

At an equivalent time, on their own, outside an infected host, viruses are more “dead” than “alive,” since they're a protein “package,” containing specific genetic material.

Though not clearly “dead” or “alive,” viruses can exploit certain biological mechanisms to preserve their integrity and are more likely to duplicate.

In a new study that used both human biological samples and mice, researchers from Stockholm University and Karolinska Institutet in Solna, Sweden, are watching one such phenomenon that permits viruses to become more infectious, namely, the formation of a “protein corona.”

Viruses grow more infectious and dangerous?

In their study paper — which appears in Nature Communications — the authors explain that “[t]he terms ‘protein corona’ refers to the layer of proteins that adhere to the surfaces of nanostructures once they encounter biological fluids.”

Similarly to nanoparticles, when viruses inherit contact with biological fluids, such as blood or lung fluid, they “pick up” proteins, forming a “coating” that protects them and, thus, helps they become more harmful.

“Imagine a ball falling into a bowl of milk and cereals,” says study author Karim Ezzat.

“The ball is instantly covered by the sticky particles within the mix, and that they remain on the ball once you take it out of the bowl.”

“The same thing happens when an epidemic gets in touch with blood or lung fluids that contain thousands of proteins,” Ezzat explains.

“Many of those proteins immediately stick with the viral surface, forming a so-called protein corona.”

To begin with, the researchers checked out how acquiring a protein corona influenced the respiratory syncytial virus (RSV), a standard virus that causes acute respiratory infections, especially in children.

Ezzat notes that his and his colleagues’ analysis revealed that “[t]he protein corona signature of RSV within the blood is extremely different from that in the lung fluids.”

“It is additionally different between humans and other species, like rhesus macaque monkeys, which can also, be infected with RSV,” he adds.

“The virus remains unchanged on the genetic level.

It just acquires different identities by accumulating different protein coronae on its surface, counting on its environment.

This makes it possible for the virus to use extracellular host factors for its benefit, and we’ve shown that a lot of those different coronae make RSV more infectious,” Ezzat elaborates.

Going further, the researchers saw that infecting mice with RSV or the herpes simplex virus type 1 (HSV-1) had another effect — the viruses could bind to amyloid proteins, the sort of proteins that form toxic plaques within the brains of individuals with Alzheimer’s and other sorts of dementia.

More specifically, HSV-1 can bind to soluble amyloid proteins and facilitate their development into “threads” which will then form tangles and plaques.

And when the researchers infected the brains of mouse models “primed” for Alzheimer’s disease with HSV-1, they found that the mice developed the neurodegenerative condition within 48 hours of exposure.

Without HSV-1, the investigators explain, the experimental mice would typically take months to develop Alzheimer’s disease.

However, consistent with the authors of this study, the present findings could actually help scientists come up with better vaccines to counter such potent viruses, also as offer further insight into the factors that influence the event of neurodegenerative conditions.

“The novel mechanisms described in our paper can have an impression not only on understanding new factors determining how infectious an epidemic is but also on devising new ways to style vaccines” says Ezzat.