The Rabies lyssavirus glycoprotein (RABV-G) is largely responsible for the neuroinvasiveness of the virus and the induction of antiviral immune responses.

To study the effects of RABV-G we compared the G of the attenuated RABV variant SPBN with that of the pathogenic DOG4 strain. Infection via the olfactory route caused 100% mortality in mice with both virus variants. Of note, with the attenuated SPBN, progression of the disease was accelerated, microglia response less pronounced and IL-6 expression higher than in the presence of RABV-G from the pathogenic DOG4.

However, while virus spread was less extensive, viral gene expression in individual neurons was actually higher in SPBN–infected brains without causing apoptosis of infected neurons. These differences between the two variants were not observed in infected neuronal cultures indicating that the effects of RABV-G on virus spread and viral gene expression depend on factors only present in the intact brain.

狂犬病狂犬病毒糖蛋白（RABV-G）在很大程度上负责病毒的神经侵袭和抗病毒免疫应答的诱导。

为了研究RABV-G的作用，我们将减毒的RABV变体SPBN的G与致病性DOG4菌株的G进行了比较。通过嗅觉途径感染会在两种病毒变体的小鼠中造成100％的死亡率。值得注意的是，与减毒的SPBN相比，病原性DOG4引起的小胶质细胞反应加快，小胶质细胞反应不明显，IL-6表达更高。

但是，尽管病毒的传播范围较小，但在受SPBN感染的大脑中，单个神经元中病毒基因的表达实际上更高，而不会引起被感染神经元的凋亡。在感染的神经元培养物中未观察到两个变体之间的这些差异，表明RABV-G对病毒传播和病毒基因表达的影响取决于仅存在于完整大脑中的因子。