Herrera Rossana, Morris Michael, Rosbe Kristina, Feng Zhimin, Weinberg Aaron, Tugizov Sharof
Department of Medicine, School of Dentistry, University of California San Francisco, San Francisco, CA, United States.
Department of Otolaryngology, School of Dentistry, University of California San Francisco, San Francisco, CA, United States.
Virology. 2016 Jan;487:172-87. doi: 10.1016/j.virol.2015.09.025. Epub 2015 Nov 2.
We previously showed that expression of the anti-HIV innate proteins human beta-defensin 2 (hBD2) and hBD3 in adult oral epithelial cells reduces HIV transepithelial transmission by inactivation of virus. However, fetal/infant oral epithelia lack beta-defensin expression, leading to transmission of HIV. The mechanisms of hBD2- and hBD3-mediated HIV inactivation in adult oral epithelial cells are poorly understood. Here we found that heparan sulfate proteoglycans (HSPGs) on the apical surfaces of epithelial cells facilitate simultaneous binding of hBDs and HIV gp120 to the cell surface. HSPG-facilitated binding of hBDs and HIV gp120 to the cell surface did not affect viral attachment. HBD2 or -3 cointernalized with virions in endosomes, formed oligomers, and reduced infectivity of HIV. The anti-HIV effect of combining hBD2 and hBD3 was substantially higher than that of the individual peptides. These findings advance our understanding of the mechanisms of anti-HIV resistance in adult oral epithelium.
我们之前的研究表明,成人口腔上皮细胞中抗HIV固有蛋白人β-防御素2(hBD2)和hBD3的表达可通过使病毒失活来减少HIV的跨上皮传播。然而,胎儿/婴儿口腔上皮缺乏β-防御素表达,导致HIV传播。hBD2和hBD3介导的成人口腔上皮细胞中HIV失活机制尚不清楚。在此,我们发现上皮细胞顶端表面的硫酸乙酰肝素蛋白聚糖(HSPG)促进hBDs和HIV gp120同时结合到细胞表面。HSPG促进的hBDs和HIV gp120与细胞表面的结合不影响病毒附着。HBD2或-3与病毒粒子在内体中共内化,形成寡聚体,并降低HIV的感染性。联合使用hBD2和hBD3的抗HIV效果显著高于单个肽。这些发现增进了我们对成人口腔上皮抗HIV抗性机制的理解。