Nuclear factor (NF)-κB is a major regulator of antiviral response. Viral pathogens exploit NF-κB activation pathways to avoid cellular mechanisms that eliminate the infection. Canonical (classical) NF-κB signaling, which regulates innate immune response, cell survival and inflammation, is often manipulated by viral pathogens that can counteract antiviral response. Oncogenic viruses can modulate not only canonical, but also non-canonical (alternative) NF-κB activation pathways. The non-canonical NF-κB signaling is responsible for adaptive immunity and plays a role in lymphoid organogenesis, B cell development, as well as bone metabolism. Thus, non-canonical NF-κB activation has been linked to lymphoid malignancies. However, some data strongly suggest that the non-canonical NF-κB activation pathway may also function in innate immunity and is modulated by certain non-oncogenic viruses. Collectively, these findings show the importance of studying the impact of different groups of viral pathogens on alternative NF-κB activation. This mini-review focuses on the influence of non-oncogenic viruses on the components of non-canonical NF-κB signaling.

中文翻译：

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非致癌病毒对非经典NF-κB信号的操纵。

核因子（NF）-κB是抗病毒反应的主要调节剂。病毒病原体利用NF-κB激活途径来避免消除感染的细胞机制。规范先天性NF-κB信号传导（调节先天免疫应答，细胞存活和炎症）通常由可抵消抗病毒应答的病毒病原体操纵。致癌病毒不仅可以调节经典的，而且可以调节非经典的（替代性）NF-κB激活途径。非经典的NF-κB信号负责适应性免疫，并在淋巴器官发生，B细胞发育以及骨代谢中起作用。因此，非经典的NF-κB活化与淋巴样恶性肿瘤有关。然而，一些数据强烈表明，非经典的NF-κB激活途径也可能在先天免疫中起作用，并受某些非致癌病毒的调节。总而言之，这些发现表明研究不同组病毒病原体对替代性NF-κB活化的影响的重要性。这份小型回顾着重于非致癌病毒对非规范性NF-κB信号传导成分的影响。