流感病毒神经氨酸酶激活潜伏的转化生长因子β。
Influenza virus neuraminidase activates latent transforming growth factor beta.
作者信息
Schultz-Cherry S, Hinshaw V S
机构信息
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 53706, USA.
出版信息
J Virol. 1996 Dec;70(12):8624-9. doi: 10.1128/JVI.70.12.8624-8629.1996.
Abstract
Transforming growth factor beta (TGF-beta) is a family of proteins secreted by virtually all cells in a biologically inactive form. TGF-beta levels increase during many pathophysiological situations, including viral infection. The mechanism for increased TGF-beta activity during viral infection is not understood. We observed an increase in active TGF-beta levels within 1 day in mice infected with influenza virus. Further studies showed that the neuraminidase glycoprotein of influenza A and B viruses directly activates latent TGF-beta in vitro. There are sufficient levels of TGF-beta activated by virus to induce apoptosis in cells. In addition, influenza virus-induced apoptosis is partially inhibited by TGF-beta-specific antibodies. These novel findings suggest a potential role for activation of TGF-beta during the host response to influenza virus infection, specifically apoptosis. This is the first report showing direct activation of latent TGF-beta by a viral protein.
摘要
转化生长因子β（TGF-β）是一类由几乎所有细胞以生物无活性形式分泌的蛋白质家族。在许多病理生理情况下，包括病毒感染期间，TGF-β水平会升高。病毒感染期间TGF-β活性增加的机制尚不清楚。我们观察到感染流感病毒的小鼠在1天内活性TGF-β水平升高。进一步研究表明，甲型和乙型流感病毒的神经氨酸酶糖蛋白在体外可直接激活潜伏的TGF-β。病毒激活的TGF-β水平足以诱导细胞凋亡。此外，TGF-β特异性抗体可部分抑制流感病毒诱导的细胞凋亡。这些新发现表明，在宿主对流感病毒感染的反应中，特别是在细胞凋亡过程中，TGF-β的激活可能具有潜在作用。这是第一份显示病毒蛋白直接激活潜伏TGF-β的报告。
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