The human immunodeficiency virus (HIV) affects around 36.7 million people worldwide, according to the Joined United Nations Programme on HIV/AIDS (UNAIDS). Of these, 1.1 million people are Americans, say the Centers for Disease Control and Prevention (CDC).
Currently, there is no cure for HIV, but antiretroviral therapy (ART) allows patients to live healthier lives, reducing the risk of transmission and halting the progression of the virus as much as possible.
The National Institute of Allergy and Infectious Diseases (NIAID), one of the National Institutes of Health (NIH), make HIV research one of their top priorities with the hope of reducing the transmission rates of the virus even further.
One recent NIH study examines the way in which the virus is able to infect healthy cells by inserting its genetic material into them.
The work was conducted by Dr. Leonid V. Chernomordik, senior researcher, and other specialists, including lead author Dr. Elena Zaitseva, at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), which is part of the NIH.
The discoveries made by the specialists, potentially leading to the creation of new, more efficient virus-preventive drugs, were recently published in Cell Host & Microbe.
The researchers identified and analyzed a crucial part of the HIV transmission process, which, if prevented, can halt infection.
The infection process happens when a protein on the surface of an HIV particle binds to surface molecules of a previously healthy cell. This leads to the eventual fusion of the virus’ and the cell’s outer membranes, which allows HIV’s genetic material to enter the cell.
It was found that during this process, a protein called “transmembrane protein 16F” (TMEM 16F) becomes active. TMEM 16F transfers phosphatidylserine, a phospholipid found inside the cell membrane, to its outer surface.
Phosphatidylserine plays an important role in cell signaling, a communication process coordinating cell action. If the signaling is disrupted, then the system becomes exposed to anomalies. Previous research published in The Open Virology Journal suggested that HIV exploits cell signaling, but the results remained contested.
In the new study conducted at NICHD, researchers observed that virus molecules bind with phosphatidylserine. This is a key element facilitating the embedding of HIV genetic material into healthy cells, as phosphatidylserine’s signaling boosts the fusion process.
The team also noticed that chemically blocking the transfer of the phospholipid, or binding it to other molecules to prevent a bond with those of HIV, can prevent fusion. In this way, the process of infection is interrupted.
“Our findings suggest that the ability of the cells to mount PS [phosphatidylserine] signaling is an important aspect of immune cell activation and one of the controlling mechanisms for both productive and aborted infection of the cells.”
Dr. Elena Zaitseva et al.
The researchers suggest that this discovery might lead to the development of much more effective HIV treatments, focused on disrupting the transmission of HIV genetic material to cells.
Though this gives new hope in the battle against HIV, the improved treatment still lies far ahead in the future. Further studies are needed to perfect our understanding of the virus, the researchers note.