Protein May Block Release of Ebola Virus, HIV

A family of proteins that promotes the entry of viruses into cells may be able to block the release of Ebola, HIV, and other viruses, according to a study authored by researchers at the University of Missouri (MU).

When any virus infects a cell, it subsequently replicates and spreads to other cells, the investigators determined. Their study revealed the cellular protein T-cell immunoglobulin and mucin domain (TIM-1), which was previously found to promote the entry of some pathogenic viruses into host cells, might be able to block the release of the Ebola virus and HIV.

“This is a surprising finding that provides new insights into our understanding of not only HIV infection, but also that of Ebola and other viruses,” said Shan-Lu Liu, MD, PhD, associate professor in the MU School of Medicine’s Department of Molecular Microbiology and Immunology, in a press release.

To date, the most recent outbreak has caused more than 1400 fatalities with more than 2600 confirmed and suspected cases, according to the US Centers for Disease Control and Prevention.

The study showed that TIM-1 proteins are able to prevent viral particles from being released by an infected cell by keeping it tied to the cell’s surface, which could potentially slow viral production. The researchers noted that this ability to inhibit viral particles applies to several enveloped viruses, including HIV and Ebola.

The study involved a variety of experiments that demonstrated the protein family’s ability to block the release of HIV, which led to decreased viral production and replication. The researchers noted that a virus like HIV attacks cells that are vital to the body’s immune system and disrupts the ability of white blood cells to respond to the infection. As the viral particles attempt to exit the infected cell, however, the TIM-family proteins that are located on the cellular surface can attach to the lipids on the surface of the viral particle.

Those lipids, which are usually on the inside of cellular membrane, can potentially be exposed to the outside once viral infection occurs. The viral particle then attaches to the host cell, which prevents the particle from being released from the cell. Finally, the viral particles get stuck to one another to form a network of viral particles on the surface of the host cell, instead of infecting other cells, according to the study.

“We are not at the point to draw a conclusion as to whether this is a positive or a negative factor,” Dr. Liu said. “However, this discovery furthers our ultimate goal of understanding the biology of TIM-family proteins and potentially developing applications for future antivirus therapies.”