HIV-1 attacks cells that are vital to the body's immune system, such as T cells. These white blood cells play an important role in the body's response to infection, but HIV-1 disrupts the cells' ability to fight back against infection. When the virus enters a host cell, it infects the cell and replicates, producing viral particles that spread to and infect other cells. The researchers found that as the viral particles attempt to bud from, or leave, the infected cell, the TIM-family proteins located on the surface of the cell can attach to lipids on the surface of the viral particle.
These lipids known as phosphatidylserine (PS) are normally present on the inner side of the cellular membrane but can be exposed to the outer side upon viral infection. When the TIM-family proteins come in contact with PS, the viral particle becomes attached to the host cell, keeping the particle from being released from the cell. Because TIM-family proteins and PS are present on the surface of the cell and the viral particle, the viral particles get stuck to one another, forming a network of viral particles that accumulate on the surface of the host cell, rather than being released to infect other cells.
By using molecular, biochemical and electron microscopic approaches, the researchers observed the TIM and PS interactions in human cells. The next step is for the researchers to study the biological significance of TIM-family proteins in animals and patients and to determine the fate of the infected cell once it accumulates a buildup of viral particles.
"We are not at the point to draw a conclusion as to whether this is a positive or a negative factor," Liu said. "However, this discovery furthers our ultimate goal of understanding the biology of TIM-f
|Contact: Derek Thompson|
University of Missouri-Columbia