Scientists discover ‘window of opportunity’ against the virus

Scientists discover ‘window of opportunity’ against the virus
Scientists discover ‘window of opportunity’ against the virus
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The human immunodeficiency virus (HIV) causes an infection that attacks the immune system. Acquired immunodeficiency syndrome (AIDS) is the most advanced stage. According to the World Health Organization (WHO), HIV is still a global public health problem. By mid-2023, the agent had caused more than 40 million deaths. While current care focuses on prevention and control, scientists look for weaknesses in the virus to find a cure or vaccines. Aiming to better understand HIV, researchers at Duke University in the United States noticed ultra-fast movement on the surface of the virus. Antibodies targeting this mobile part could be key to a vaccine approach.

As HIV moves out of a human cell to attack and spread its genetic payload, there is a quick moment when a small piece of its surface breaks open to begin the infection process. Noticing the opening and closing of this structure in millionths of a second gave researchers at Duke University’s Human Vaccine Institute a new understanding of the virus’s surface that could lead to the production of antibodies for an AIDS vaccine. The results of the trial were detailed yesterday in the magazine Science Advances.

Alternative

According to researchers, being able to bind an antibody to this tiny part, preventing it from opening, would be crucial. The mobile piece is a structure called envelope glycoprotein, and researchers have been trying to understand it for a long time, as it is essential for the virus to dock with a T cell receptor — essential for the immune system — known as CD4. Many pieces of the envelope are constantly moving to avoid the immune system.

“Everything everyone has done to try to stabilize this structure will not work, because of what we have learned,” said lead author Rory Henderson, a structural biologist and professor of medicine at the university, in a note. “It’s not that they did anything wrong, it’s just that we didn’t know she moved that way.”

Postdoctoral researcher and study co-author, Ashley Bennett, details the results found. According to her, as the virus searches for the best point of attachment on a human T cell, the first point of contact is the host cell’s CD4 receptor. This connection is what triggers the opening of the envelope structure, exposing a binding site for coreceptors, “and that’s the event that really matters.”

When the virus molecules are bound to the cell membrane, the viral RNA injection process can begin. “If it gets into the cell, its infection is now permanent,” Henderson said. “If you get infected, you’ve already lost the game because it’s a retrovirus”, reinforced Bennett.

The mobile structure discovered by the team protects the co-receptor binding site on the virus. “It’s also a lock to stop it from opening until it’s ready to open,” Henderson stressed. According to the researcher, maintaining the lock with a specific antibody would interrupt the infection process.

Josias Aragão, an infectious disease specialist at the Hospital do Servidor Público Estadual, in São Paulo, considers that, despite the relevance of the discovery, there is still a lot to understand, as HIV has several factors that make a cure difficult.

“This also depends on the interaction of the virus with the host. This difficulty has to do with the interaction of the virus with the person who carries it. HIV has mechanisms that allow it to escape the immune system. Part of its genetic material becomes integrated with the material human genetics. There is also great viral diversity within the same individual, with subpopulations of the virus in different systems and organs.”

Process

To analyze the virus in opening, closing and intermediate phases, the authors used an electron accelerator located at the Argonne National Laboratory in the United States. To obtain the information they needed, they had access to three periods of 120 hours with the equipment.

Previous work suggested that antibodies were being engineered into the wrong shapes on the virus, the new trial reveals this was probably correct. “The question was ‘why, when we immunize, are we getting antibodies to places that should be blocked?'” Henderson asked. Part of the answer must be found in this structure and its ability to transform.

“The interplay between antibody binding and what that shape represents is really crucial to the work we do. It led us to design an immunogen the day we got back from the first experiment. We think we know how it works,” concluded the author. main.

Marcelo Neubauer, infectious disease specialist and member of the Brazilian Medical College of Acupuncture (CMBA), emphasizes the need to remember the importance of controlling the pathogen. “Currently, we are able to keep the patient symptom-free, with an undetectable viral load and an adequate number of defense cells. However, thinking about a cure is very difficult. Furthermore, the idea of ​​a vaccine is quite complex, given the characteristics of the virus itself, which act on the defense system. In a way, a vaccine could stimulate the virus to reach more defense cells.”

Prevention

“Several vaccines have already been studied and none have gone forward, acting in different locations. But this could be a new opportunity, with a new location to be studied, to create a vaccine that may work. This is very interesting. Today we have treatment with which a person lives with HIV and has an undetectable viral load, due to medications they do not transmit it. This is already a form of prevention, there is also prep, which is pre-exposure prophylaxis, a similar combination of medications, but not equal to the cocktail of virus carriers.”

Juliana Fenleyinfectious disease specialist and medicine coordinator at Anhembi Morumbi University

Prevention

“Several vaccines have already been studied and none have gone forward, acting in different locations. But this could be a new opportunity, with a new location to be studied, to create a vaccine that may work. This is very interesting. Today we have treatment with which a person lives with HIV and has an undetectable viral load, due to medications they do not transmit it. This is already a form of prevention, there is also prep, which is pre-exposure prophylaxis, a similar combination of medications, but not equal to the cocktail of virus carriers.”

Juliana Fenley, infectious disease specialist and medicine coordinator at Anhembi Morumbi University

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The article is in Portuguese

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