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Geometry goes viral: Researchers use maths to solve virus puzzle

Geometry goes viral: Researchers use maths to solve virus puzzle

Researchers have developed a new mathematical framework that changes the way we understand the structure of viruses such as Zika and Herpes.

The new mathematical framework changes the way we understand the structure of viruses such as Herpes.

The discovery, by researchers at the University of York (UK) and San Diego State University (US), paves the way for new insights into how viruses form, evolve and infect their hosts and may eventually open up new avenues in anti-viral therapy.

Viruses look like tiny footballs because they package their genetic material into protein containers that adopt polyhedral shapes.

The new theory revolutionises our understanding of how these containers are shaped, solving a scientific mystery that has endured for half a century.

High resolution

For more than fifty years, scientists have followed the Caspar-Klug theory (CKT) about how the protein containers of viruses are structured. However, improvements in our ability to image viral particles at high resolution have made it apparent that many virus structures do not conform to these blueprints.

Published in the journal Nature Communications, the new theory accurately predicts the positions of proteins in the containers of all icosahedral (or twenty-sided) for the first time. It simultaneously works for viruses that conform to CKT and for those that posed an unresolved problem to that theory.

Professor Reidun Twarock, mathematical biologist at the University of York’s departments of Mathematics and Biology and a member of the York Cross-disciplinary Centre for Systems Analysis, said: “Our study represents a quantum leap forward in the field of structural virology, and closes gaps in our understanding of the structures of many viruses that are ill described by the existing framework.

Anti-viral strategies

“This theory will help scientists to analyse the physical properties of viruses, such as their stability, which is important for a better understanding of the mechanism of infection. Such insights can then be exploited for the development of novel anti-viral strategies.

“In particular the structures of larger and more complex viruses that are formed from multiple different components were previously not well understood.

“Our over-arching scheme reveals container architectures with protein numbers that are excluded by the current framework, and thus closes the size gaps in CKT.

Viral evolution

“The new blueprints also provide a new perspective on viral evolution, suggesting novel routes in which larger and more complex viruses may have evolved from simple ones at evolutionary timescales.”

Dr Antoni Luque, theoretical biophysicist at San Diego State University and their Viral Information Institute, said: “We can use this discovery to target both the assembly and stability of the capsid, to either prevent the formation of the virus when it infects the host cell, or break it apart after it’s formed. This could facilitate the characterization and identification of antiviral targets for viruses sharing the same icosahedral layout.”

Materials provided by the University of York


Deadly protein duo reveals new drug targets for viral diseases

It sounds like a plot point from a sci-fi movie: Two different and dangerous monsters merge into a hybrid that is more powerful and deadly than either counterpart.

Yet a research team led by Hector Aguilar-Carreno, associate professor in the Department of Microbiology and Immunology, has found a potentially similar scenario with a pair of viruses, in a study published July 31 in the Journal of Virology.

Their paper – featured on the journal’s cover in July – details how two highly lethal viruses (Nipah and Hendra) have greater pathogenic potential when their cell-sabotaging proteins are combined.

“Co-infections with these two viruses can occur in the same host, but we didn’t know what would happen if their proteins combined,” Aguilar-Carreno said. “We discovered that not only could they work together, they can work even better than they do separately.”

Members of the Aguilar-Carreno research team are experts on how Nipah and Hendra viruses attach to, and fuse with, their hosts’ cells. The viruses’ natural host is the fruit bat; this relationship was captured in an illustration, chosen for the journal cover, by Aguilar-Carreno’s husband, Armando Pacheco, a Cornell Institute of Biotechnology staff member.

The researchers’ focus is on the viral fusion proteins (or F proteins) and attachment proteins (G proteins). In previous studies, the team unveiled how the two proteins physically interact to enable viral infections: A G protein attaches to the cell; G then triggers F to flip up and down, triggering fusion between the cellular and viral membranes – the first moment of infection.

Aguilar-Carreno knew this “dance” between G and F was a crucial step in viral infection, but was curious to know how the dance might change if the proteins got new partners. Since both Nipah and Hendra viruses can potentially co-infect fruit bats, a protein partner switch is likely to occur in the wild.

He and his team tested out different Nipah-Hendra protein combinations in the lab, using genetic approaches in human cells. In some pairings, the two gripped each other in a tight, tango-like embrace. But one hybrid – a Hendra F and Nipah G – behaved like Lindy Hoppers, allowing the F protein to perform “aerials” that heightened fusion between the virus and the cell.

“This combination of proteins had a looser interaction,” Aguilar-Carreno said. “This looseness actually corresponded to greater fusion capability – and therefore an implied greater” ability to cause disease.

This hybrid protein power-couple has interesting implications.

“I find it fascinating – the tightness of the interaction is so crucial for these two proteins,” Aguilar-Carreno said. “If they’re too tight, they can’t coordinate correctly to get into the cell. And now that we know this, we can leverage that to stop viral-cell fusion.”

Aguilar-Carreno said this kind of therapeutic approach might be used to improve vaccine efficacy, or as an alternative to vaccines. His lab is working on vaccine approaches on animal models, as well as therapeutic approaches informed by this new discovery.

Aguilar-Carreno’s lab is also working on related research that may lead to vaccine-free therapies or improved vaccines to treat enveloped viruses, which include infectious diseases such as human immunodeficiency virus (HIV) and influenza. Enveloped viruses are wrapped in an outer coat made from a piece of the infected cell’s plasma membrane, which may protect the virus and help it infect other cells.

“Our work could lead to drugs,” Aguilar-Carreno said, “that enable inventions such as a flu vaccine with broader protection and greater efficacy.”

Journal Reference: Journal of Virology

Materials provided by Cornell University

most dangerous malwares, an illustration of viruses

Laptop with six most dangerous malwares sold for 1.3 million dollars

No one wants to use a laptop infected with computer viruses, right? What about a laptop with the six most dangerous computer malware ever, installed in it? Well, it just sold for 1.3 million USD at an online auction.

The laptop named “The Persistence of Chaos” has been created by Chinese artist Guo O Dong. The buyer is anonymous but there is a lot of information about the laptop. Dong collaborated with a cybersecurity company, Deep Instinct to load the laptop with the dangerous viruses. Deep Instinct is the first company to use deep learning technology for cybersecurity and it can detect even unknown malware across all range of devices.

The laptop is an ordinary 10.2 inch Samsung NC10-14GB running Windows XP. It is airgapped which means that it cannot be used for connecting to other networks. The 6 pieces of malware running in it have caused financial damages totalling 95 billion USD in the past.

The 6 malware are ILOVEYOU, MyDoom, SoBig, WannaCry, DarkTequila and BlackEnergy.

Guo commented that these softwares may seem abstract with their funny names, but it emphasizes the fact that web and real life are not separate spaces. Malware is a significant way to demonstrate how the apparently fun and harmless Internet can create a huge mess in your real life.

ILOVEYOU is a virus that was distributed through e-mail and virtual file sharing, affecting almost 500,000 machines and causing damage of 15 billion USD. It came with the email subject header “ILOVEYOU” and deleted the local files in the machine when executed.

MyDoom was created by Russian spammers and it remains the fastest spreading worm till date. It targeted specific servers and the damage caused by it is projected to be 38 billion USD.

SoBig remains the second fastest computer worm only surpassed by MyDoom. It is not only a computer worm, spreading by self-replication but also a Trojan Horse pretending to be some other application.

WannaCry is a ransomware cryptoworm which targeted machines running Windows operating system. It encrypted files and asked for ransom payments to be made through Bitcoins.

DarkTequila is a complex malware running mainly in Latin American countries intended to steal financial information as well as login credentials of popular websites. And finally, there is BlackEnergy which is a web toolkit designed to execute DDoS attacks. In December 2015, it caused a huge blackout in Ukraine.

The laptop has been live-streamed online to make sure no sudden moves are performed. It may seem absurd that an old laptop is fetching so much money but according to Guo, he thinks of the artwork as a catalogue of historical threats.

After listening to this news, I think that many of you would be interested in getting malware into your laptops and then selling them. Tell us what do you think, with a short and quick comment.