According to recent research in vitro and in mice, viruses that come into 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, such as Alzheimer’s.
Research shows that viruses can acquire a protein ‘coating’ that makes them more infectious.
Viruses are strange, fascinating agents, not least because scientists still find it difficult to say whether they qualify as living organisms or not.
To replicate, viruses have to infect a host — so in a live biological environment, viruses are also “alive,” interacting with the cells of the host they infect and multiplying.
At the same time, on their own, outside an infected host, viruses are more “dead” than “alive,” since they are a protein “package,” containing specific genetic material.
Though not clearly “dead” or “alive,” viruses can exploit certain biological mechanisms to preserve their integrity and be more likely to replicate.
In a new study that used both human biological samples and mice, researchers from Stockholm University and Karolinska Institutet in Solna, Sweden, have been looking at one such phenomenon that allows viruses to become more infectious, namely, the formation of a “protein corona.”
In their study paper — which appears in Nature Communications — the authors explain that “[t]he term ‘protein corona’ refers to the layer of proteins that adhere to the surfaces of nanostructures when they encounter biological fluids.”
Similarly to nanoparticles, when viruses come into contact with biological fluids, such as blood or lung fluid, they “pick up” proteins, forming a “coating” that protects them and, thus, helps them become more harmful.
“Imagine a tennis ball falling into a bowl of milk and cereals,” says study author Kariem Ezzat. “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,” Ezzat explains. “Many of these proteins immediately stick to the viral surface, forming a so-called protein corona.”
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To begin with, the researchers looked at how acquiring a protein corona influenced the respiratory syncytial virus (RSV), a common 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 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,” he adds.
“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’ve shown that many of these 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 type of proteins that form toxic plaques in the brains of people with Alzheimer’s and other forms of dementia.
More specifically, HSV-1 can bind to soluble amyloid proteins and facilitate their development into “threads” that can then form tangles and plaques.
And when the researchers infected the brains of mouse models “primed” for Alzheimer’s diseasewith 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, according to the authors of this study, the current findings could actually help scientists come up with better vaccines to counter such potent viruses, as well as offer further insight into the factors that influence the development of neurodegenerative conditions.
“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,” says Ezzat.
“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.”