Schmallenberg virus (SBV) induces fetal malformation, abortions and stillbirth in ruminants. While the non-structural protein NSs is a major virulence factor, the biological function of NSm, the second non-structural protein which consists of three hydrophobic transmembrane (I, III, V) and two non-hydrophobic regions (II, IV), is still unknown. Here, a series of NSm mutants displaying deletions of nearly the entire NSm or of the non-hydrophobic domains was generated and the intracellular distribution of NSm was assessed. SBV-NSm is dispensable for the generation of infectious virus and mutants lacking domains II – V showed growth properties similar to the wild-type virus. In addition, a comparable intracellular distribution of SBV-NSm was observed in mammalian cells infected with domain II mutants or wild-type virus. In both cases, NSm co-localized with the glycoprotein Gc in the Golgi compartment. However, domain IV-deletion mutants showed an altered distribution pattern and no co-localization of NSm and Gc.

Schmallenberg病毒（SBV）引起反刍动物胎儿畸形，流产和死产。非结构蛋白NSs是主要的致病因子，而NSm的生物学功能是第二个非结构蛋白，它由三个疏水性跨膜（I，III，V）和两个非疏水性区域（II，IV）组成，仍然未知。在这里，产生了一系列NSm突变体，这些突变体显示出几乎整个NSm或非疏水域的缺失，并评估了NSm在细胞内的分布。SBV-NSm对于产生传染性病毒是必不可少的，缺少II-V结构域的突变体显示出与野生型病毒相似的生长特性。此外，在感染了结构域II突变体或野生型病毒的哺乳动物细胞中观察到了SBV-NSm的可比细胞内分布。在这两种情况下 NSm与高尔基区中的糖蛋白Gc共定位。但是，域IV删除突变体显示改变的分布模式，并且没有NSm和Gc的共定位。