Marvin Shauna A, Huerta C Theodore, Sharp Bridgett, Freiden Pamela, Cline Troy D, Schultz-Cherry Stacey
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA Rhodes College, Memphis, Tennessee, USA.
J Virol. 2015 Dec 9;90(4):1988-96. doi: 10.1128/JVI.02367-15. Print 2016 Feb 15.
Little is known about intrinsic epithelial cell responses against astrovirus infection. Here we show that human astrovirus type 1 (HAstV-1) infection induces type I interferon (beta interferon [IFN-β]) production in differentiated Caco2 cells, which not only inhibits viral replication by blocking positive-strand viral RNA and capsid protein synthesis but also protects against HAstV-1-increased barrier permeability. Excitingly, we found similar results in vivo using a murine astrovirus (MuAstV) model, providing new evidence that virus-induced type I IFNs may protect against astrovirus replication and pathogenesis in vivo.
Human astroviruses are a major cause of pediatric diarrhea, yet little is known about the immune response. Here we show that type I interferon limits astrovirus infection and preserves barrier permeability both in vitro and in vivo. Importantly, we characterized a new mouse model for studying astrovirus replication and pathogenesis.
关于上皮细胞对星状病毒感染的内在反应知之甚少。在此我们表明，1型人星状病毒（HAstV-1）感染可诱导分化的Caco2细胞产生I型干扰素（β干扰素[IFN-β]），这不仅通过阻断正链病毒RNA和衣壳蛋白合成来抑制病毒复制，还能防止HAstV-1增加的屏障通透性。令人兴奋的是，我们在使用鼠星状病毒（MuAstV）模型的体内实验中发现了类似结果，这为病毒诱导的I型干扰素可能在体内预防星状病毒复制和发病机制提供了新证据。
人星状病毒是小儿腹泻的主要病因，但对其免疫反应了解甚少。在此我们表明，I型干扰素在体外和体内均能限制星状病毒感染并维持屏障通透性。重要的是，我们鉴定了一种用于研究星状病毒复制和发病机制的新型小鼠模型。
