Proteins that help entry HIV, Ebola viruses also block their release: Study

Washington: In a surprise finding,scientists have discovered that a family of proteins thathelps viruses, such as HIV and Ebola, enter a cell can alsoblock the release of these deadly viruses. [caption id="attachment_1681131" align="alignnone" width="380"] Representational image, Reuters[/caption]"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, associate professor in the University of Missouri School of Medicine's Department of Molecular Microbiology and Immunology.AIDS is a condition characterised by progressive failureof the immune system. It is caused by the humanimmunodeficiency virus type 1 (HIV-1). When HIV-1 or any virus infects a cell, it replicates and spreads to other cells. One type of cellular protein - T cellimmunoglobulin and mucin domain, or TIM-1 - has previouslybeen shown to promote entry of some highly pathogenic virusesinto host cells.Now, researchers have found that the same proteinpossesses a unique ability to block the release of HIV-1 andEbola virus. "This study shows that TIM proteins keep viral particlesfrom being released by the infected cell and instead keep themtethered to the cell surface," said Gordon Freeman, associateprofessor of medicine with Harvard Medical School'sDana-Farber Cancer Institute. "This is true for several important enveloped viruses including HIV and Ebola. We may be able to use this insight to slow the production of these viruses," said Freeman.Under the supervision of Liu, Minghua Li, a graduatestudent in the MU Pathobiology Area Programme, performed aseries of experiments that revealed the protein's ability toinhibit HIV-1 release, resulting in diminished viralproduction and replication.HIV-1 attacks cells that are vital to the body's immunesystem, such as T cells. These white blood cells play animportant role in the body's response to infection, but HIV-1disrupts the cells' ability to fight back against infection.When the virus enters a host cell, it infects the celland replicates, producing viral particles that spread to andinfect other cells.The researchers found that as the viral particles attemptto bud from, or leave, the infected cell, the TIM-familyproteins located on the surface of the cell can attach tolipids 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 theparticle from being released from the cell.Because TIM-family proteins and PS are present on thesurface of the cell and the viral particle, the viralparticles get stuck to one another, forming a network of viralparticles that accumulate on the surface of the host cell,rather than being released to infect other cells.The study was published in the journal PNAS. PTI