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HIV is believed to have evolved from a simian immunodeficiency virus SIV, that originated in chimpanzees, a crucial protein for protection acts as a sticky pad on the surface of infected cells, preventing them from releasing nascent virus particles. Viruses have developed their protection of proteins as a countermeasure. Vpu, an HIV accessory protein that targets tetherin, allows HIV to escape and spread.
An international team led by Kei Sato and Yoshio Koyanagi of Kyoto University set out to test whether the evolution of Vpu could have aided SIV in making the leap to humans. Researchers used an immunodeficient mouse model with a reconstituted human immune system, established through the transplantation of human blood-forming stem cells. Using reverse genetics to engineer several HIV strains with different Vpu mutants, the team investigated which Vpu function was key for successful virus infection.
Vpu can inhibit immune signaling pathways in the cell and degrade tetherin, the Vpu variant responsible for downregulating tetherin was the most important property of Vpu for HIV. Returning tetherin to normal levels could suppress virus replication, suggesting that a minimal number of tetherin molecules can combat HIV. SIV could not effectively infect human blood cells in the mouse model. But when SIV Vpu was endowed with properties resembling HIV Vpu.
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