Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, India.
Viruses. 2024 Aug 29;16(9):1383. doi: 10.3390/v16091383.
Autophagy, an evolutionarily conserved cellular process, influences the regulation of viral infections. While the existing understanding indicates that Herpes Simplex Virus type 2 (HSV-2) maintains a basal level of autophagy to support its viral yield, the precise pathways governing the induction of autophagy during HSV-2 infection remain unknown. Therefore, this study aims to explore the role of type I interferons (IFN-I) in modulating autophagy during HSV-2 infection and to decode the associated signaling pathways. Our findings revealed an interplay wherein IFN-I regulates the autophagic response during HSV-2 infection. Additionally, we investigated the cellular pathways modulated during this complex process. Exploring the intricate network of signaling events involved in autophagy induction during HSV-2 infection holds promising therapeutic implications. Identifying these pathways advances our understanding of host-virus interactions and holds the foundation for developing targeted therapeutic strategies against HSV-2. The insight gained from this study provides a platform for exploring potential therapeutic targets to restrict HSV-2 infections, addressing a crucial need in antiviral research.
自噬是一种进化上保守的细胞过程,影响病毒感染的调控。虽然现有研究表明单纯疱疹病毒 2 型 (HSV-2) 维持基础水平的自噬以支持其病毒产量,但在 HSV-2 感染期间诱导自噬的确切途径仍不清楚。因此,本研究旨在探讨 I 型干扰素 (IFN-I) 在调节 HSV-2 感染期间自噬中的作用,并解码相关的信号通路。我们的研究结果揭示了 IFN-I 在 HSV-2 感染期间调节自噬反应的相互作用。此外,我们还研究了在这个复杂过程中被调节的细胞途径。探索 HSV-2 感染期间诱导自噬的信号事件的复杂网络具有潜在的治疗意义。鉴定这些途径有助于我们理解宿主-病毒相互作用,并为开发针对 HSV-2 的靶向治疗策略奠定基础。本研究提供了一个探索限制 HSV-2 感染的潜在治疗靶点的平台,这是抗病毒研究的一个关键需求。