An unexpected, pH-sensitive step of the enterovirus D68 lifecycle.
An unexpected, pH-sensitive step of the enterovirus D68 lifecycle.
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肠道病毒D68(EV-D68)可引起病原体引起的呼吸系统疾病和严重的神经系统疾病，如急性弛缓性脊髓炎。我们缺乏EV-D68预防措施，对其分子和细胞生物学的了解也不完整。多项研究强调了膜间隔和自噬在微小核糖核酸病毒增殖过程中的作用。Galitska等人。发现EV-D68也利用细胞自噬间隔并依赖自噬机制作为亲病毒因子(G.Galitska，A.Jassey，M.A.Wagner，N.Pollack等，mBioe02141-23,2023年，https://doi.org/10.1128/mbio.02141-23).令人惊讶的是，在EV-D68感染期间，自噬隔间未能在早期酸化，导致RNA合成延迟，这在其他肠道病毒中尚未报道。这种延迟似乎反映了病毒蛋白2B和3A不能稳定地与膜结合，导致它们在细胞质中降解。这样的观察结果强调了研究病毒属个体成员的重要性。了解这一现象与EV-D68致病机制之间的关系将是一件很有趣的事情。
Enterovirus D68 (EV-D68) contributes significantly to pathogen-induced respiratory illnesses and severe neurological disorders like acute flaccid myelitis. We lack EV-D68 preventive measures, and knowledge of its molecular and cellular biology is incomplete. Multiple studies have highlighted the role of membrane compartments and autophagy during picornavirus multiplication. Galitska et al. found that EV-D68 also exploits cellular autophagic compartments and relies on autophagic machinery as pro-viral factors (G. Galitska, A. Jassey, M. A. Wagner, N. Pollack, et al., mBio e02141-23, 2023, https://doi.org/10.1128/mbio.02141-23). Surprisingly, failure of the autophagic compartment to acidify early during EV-D68 infection causes a delay in RNA synthesis that has not been reported for other enteroviruses. This delay appears to reflect the inability of viral proteins 2B and 3A to engage membranes stably, leading to their degradation in the cytoplasm. Observations like this underscore the importance of studying individual members of the virus genus. It will be interesting to understand how this phenomenon connects to EV-D68 pathogenesis, if at all.
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