TIM-family proteins also have the ability to block the release of HIV and other viruses

TIM-family proteins also have the ability to block the release of HIV and other viruses -

TIM-family proteins also play a role in Ebola and other infections viral

a family of proteins that promotes the entry of the virus into cells also has the ability to block the release of HIV and other viruses, University of Missouri researchers have found.

"This is a surprising discovery that offers new perspectives for our understanding not only of HIV infection but also that of Ebola and other viruses," said Shan-Lu Liu, MD, Ph.D., associate professor in the school of MU Department of molecular Microbiology and immunology in medicine.

the study was recently published in Academy Acts national science . Liu, corresponding author of the study, is also an investigator with the life sciences Center at MU Christopher S. Bond.

estimated the Centers for Disease Control and Prevention, more than one million Americans are currently living with AIDS. AIDS, which is the acquired immunodeficiency syndrome, is a condition characterized by progressive failure of the immune system. it is caused by human virus type 1 immunodeficiency (HIV-1).

When HIV-1 or any virus infects a cell, it replicates and spreads to other cells. One type of cell protein - T cell immunoglobulin and mucin the field, or TIM-1 - has previously been shown to promote the entry of certain highly pathogenic viruses in host cells. Now, MU researchers found that the same protein has a unique ability to block the release of HIV-1 and Ebola virus.

"This study shows that the TIM proteins keep the viral particles to be released by the infected cell and instead of keeping them attached to the cell surface," said Gordon Freeman, Ph.D., associate professor of medicine at the Dana-Farber Cancer Institute at Harvard medical School who was not affiliated with the study. "This is true for several important enveloped viruses, including HIV and Ebola. We may be able to use this knowledge to slow production of these viruses."

Under the supervision of Liu Minghua Li, a graduate student in pathobiology MU Zone Program, conducted a series of experiments that revealed the ability of the protein to inhibit HIV-1 release, resulting decreased production and viral replication.

HIV-1 attacks cells that are vital for the body's immune system such as T lymphocytes These cells play an important role in the response of the body to infection, but the HIV- 1 disrupts the cells' ability to defend against infection. When the virus enters a host cell it infects the cell and replicates, producing viral particles that spread and infect other cells. The researchers found that the viral particles budding from trying, or leave the infected cell, the TIM-family protein located on the cell surface can bind to lipids on the surface of the viral particle.

these lipids - known as phosphatidylserine (PS) - are normally present on the inner face of the cell membrane, but can be exposed to the outside during a viral infection. When the TIM family in contact with the PS proteins, viral particle becomes attached to the host cell, maintaining the particle to be released from the cell. Because the TIM family and PS proteins are present on the surface of the cell and the viral particle, the viral particles become stuck to each other, forming a network of viral particles accumulated on the surface of the host cell rather than be released to infect other cells.

using biochemical and molecular electron microscopic approaches, the researchers observed the interaction TIM and PS in human cells. The next step 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 builds up an accumulation of viral particles.

"We are not at the point of reaching a conclusion as to whether this is positive or a negative factor," said Liu. "However, this discovery strengthens our ultimate goal of understanding the biology of TIM-family protein and potentially develop applications for future antivirus treatment."