Department of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19438, USA.
Viruses. 2009 Dec;1(3):832-51. doi: 10.3390/v1030832. Epub 2009 Nov 9.
Like many animal viruses, those of the Rhabdoviridae family, are able to antagonize the type I interferon response and cause disease in mammalian hosts. Though these negative-stranded RNA viruses are very simple and code for as few as five proteins, they have been seen to completely abrogate the type I interferon response early in infection. In this review, we will discuss the viral organization and type I interferon evasion of rhabdoviruses, focusing on vesicular stomatitis virus (VSV) and rabies virus (RABV). Despite their structural similarities, VSV and RABV have completely different mechanisms by which they avert the host immune response. VSV relies on the matrix protein to interfere with host gene transcription and nuclear export of anti-viral mRNAs. Alternatively, RABV uses its phosphoprotein to interfere with IRF-3 phosphorylation and STAT1 signaling. Understanding the virus-cell interactions and viral proteins necessary to evade the immune response is important in developing effective vaccines and therapeutics for this viral family.
与许多动物病毒一样，弹状病毒科的病毒能够拮抗 I 型干扰素反应，并在哺乳动物宿主中引起疾病。尽管这些负链 RNA 病毒非常简单，只编码多达 5 种蛋白质，但它们在感染早期就已被完全阻断了 I 型干扰素反应。在这篇综述中，我们将讨论弹状病毒的病毒组织和 I 型干扰素逃逸，重点介绍水疱性口炎病毒（VSV）和狂犬病病毒（RABV）。尽管它们具有相似的结构，但 VSV 和 RABV 规避宿主免疫反应的机制却完全不同。VSV 依赖基质蛋白来干扰宿主基因转录和抗病毒 mRNAs 的核输出。相反，RABV 使用其磷蛋白来干扰 IRF-3 的磷酸化和 STAT1 信号转导。了解病毒-细胞相互作用和逃避免疫反应所需的病毒蛋白对于开发针对该病毒家族的有效疫苗和治疗方法非常重要。
