Tech UPTechnologyThey manage to stop the infectious capacity of the...

They manage to stop the infectious capacity of the AIDS virus

HIV, the virus that causes AIDS, has already claimed the lives of more than 35 million people. Therefore, and despite the fact that progress in its treatment has decreased mortality and has almost turned it into a chronic disease, finding a definitive cure has been one of the major objectives of modern medicine.

Now, in a study led by the University of Delaware and the University of Pittsburgh School of Medicine, a group of researchers has discovered a ‘brake’ that interferes with the development of HIV into an infectious agent. This mechanism prevents the capsid, that is, the protein coat that covers the virus, from forming.

It took seven years of detailed studies of the structure and dynamics of HIV at the beginning and end of its life cycle. The movements of the virus molecules were experimentally measured and simulated in quadrillionths of a second – much faster than the blink of an eye or the flapping of a hummingbird’s wings.

What is the structure of this virus like?

As the HIV virus develops, a cascade of events occurs that affect its structure and infectivity.

“Viruses like HIV and their constituent proteins and nucleic acid molecules are dynamic entities that are constantly expanding and shrinking. Their movements are like breathing r.” This is explained by the professor of the Department of Chemistry and Biochemistry at the University of Delaware, Tatyana Polenova.

According to Polenova, the molecules in the HIV virus operate in concert, yet each movement of the molecule occurs on different time scales – a difficult scenario to simulate.

Using cutting-edge biomedical technology, including high-end computer simulations and cryoelectron microscopy, the researchers answered a long-unanswered question: How does the final step in virus maturation occur? That is, the process by which a non-infectious immature virus turns into an infectious virus particle.

The team discovered that a key peptide (SP1) has to be in a highly mobile structure to be cut by the virus’s protease, the enzyme that acts like a blade. In simulations, the peptide resembles a thin thread.

Once the SP1 peptide is cut, the HIV virus forms its protective capsid and becomes infectious.

So how do you stop that process? The scientists showed that a certain anti-HIV inhibitor, called anti-HIV Bevirima, interacted with the SPI peptide, thus preventing this capsid of the virus from developing and, therefore, preventing it from becoming infectious.

Focusing on potential drug targets to prevent HIV from becoming infectious by disrupting virus maturation is a constant goal for the team. But, at the moment, there is no treatment to apply such a finding; so far, it is limited to the laboratory.

References: ‘Quenching protein dynamics interferes with HIV capsid maturation’. Wang M, Quinn CM, Perilla JR, Zhang H, Shirra R Jr, Hou G, Byeon IJ, Suiter CL, Ablan S, Urano E, Nitz TJ, Aiken C, Freed EO, Zhang P, Schulten K, Gronenborn AM, Polenova T. Nat Commun. (2017) doi: 10.1038 / s41467-017-01856-y.

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