这项研究结果发布在Proceedings of the National Academy of Sciences杂志上，研究关注一种叫prothymosin-alpha的小蛋白的抗HIV功能。该团队先前的研究表明，这种蛋白能够阻碍艾滋病病毒入侵细胞后的复制行为，但是直到现在，还不是很清楚具体的发生机制。
Prothymosin-α inhibits HIV-1 via Toll-like receptor 4-mediated type I interferon induction
Arevik Mosoian a,1, Avelino Teixeira a, Colin S. Burns b, Leif E. Sander a, G. Luca Gusella a, Cijiang He a, J. Magarian Blandera, Paul Klotmana, and Mary E. Klotmana
Induction of type I interferons (IFN) is a central feature of innate immune responses to microbial pathogens and is mediated via Toll-like receptor (TLR)-dependent and -independent pathways. Prothymosin-α (ProTα), a small acidic protein produced and released by CD8+ T cells, inhibits HIV-1, although the mechanism for its antiviral activity was not known. We demonstrate that exogenous ProTα acts as a ligand for TLR4 and stimulates type I IFN production to potently suppress HIV-1 after entry into cells. These activities are induced by native and recombinant ProTα, retained by an acidic peptide derived from ProTα, and lost in the absence of TLR4. Furthermore, we demonstrate that ProTα accounts for some of the soluble postintegration HIV-1 inhibitory activity long ascribed to CD8+ cells. Thus, a protein produced by CD8+ T cells of the adaptive immune system can exert potent viral suppressive activity through an innate immune response. Understanding the mechanism of IFN induction by ProTα may provide therapeutic leads for IFN-sensitive viruses.