Laboratory of Molecular Virology, School of Systems Biology, George Mason University, Manassas, VA, United States.
Department of Immunology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, United States.
Front Cell Infect Microbiol. 2018 Oct 18;8:362. doi: 10.3389/fcimb.2018.00362. eCollection 2018.
Autophagy, a highly conserved process, serves to maintain cellular homeostasis in response to an extensive variety of internal and external stimuli. The classic, or canonical, pathway of autophagy involves the coordinated degradation and recycling of intracellular components and pathogenic material. Proper regulation of autophagy is critical to maintain cellular health, as alterations in the autophagy pathway have been linked to the progression of a variety of physiological and pathological conditions in humans, namely in aging and in viral infection. In addition to its canonical role as a degradative pathway, a more unconventional and non-degradative role for autophagy has emerged as an area of increasing interest. This process, known as secretory autophagy, is gaining widespread attention as many viruses are believed to use this pathway as a means to release and spread viral particles. Moreover, secretory autophagy has been found to intersect with other intracellular pathways, such as the biogenesis and secretion of extracellular vesicles (EVs). Here, we provide a review of the current landscape surrounding both degradative autophagy and secretory autophagy in relation to both aging and viral infection. We discuss their key features, while describing their interplay with numerous different viruses (i.e. hepatitis B and C viruses, Epstein-Barr virus, SV40, herpesviruses, HIV, chikungunya virus, dengue virus, Zika virus, Ebola virus, HTLV, Rift Valley fever virus, poliovirus, and influenza A virus), and compare secretory autophagy to other pathways of extracellular vesicle release. Lastly, we highlight the need for, and emphasize the importance of, more thorough methods to study the underlying mechanisms of these pathways to better advance our understanding of disease progression.
自噬是一种高度保守的过程,有助于维持细胞内环境平衡,以应对广泛的内外刺激。经典或规范的自噬途径涉及细胞内成分和致病物质的协调降解和再循环。自噬的适当调节对维持细胞健康至关重要,因为自噬途径的改变与人类多种生理和病理状况的进展有关,即在衰老和病毒感染中。除了作为降解途径的经典作用外,自噬还出现了一种更加非传统和非降解的作用,成为一个日益受到关注的领域。这个过程被称为分泌自噬,由于许多病毒被认为利用这种途径作为释放和传播病毒颗粒的手段,因此它受到了广泛关注。此外,分泌自噬已被发现与其他细胞内途径相互作用,如细胞外囊泡 (EVs) 的生物发生和分泌。在这里,我们回顾了与衰老和病毒感染相关的降解自噬和分泌自噬的当前研究进展。我们讨论了它们的关键特征,同时描述了它们与许多不同病毒(即乙型和丙型肝炎病毒、EB 病毒、SV40、疱疹病毒、HIV、基孔肯雅热病毒、登革热病毒、寨卡病毒、埃博拉病毒、HTLV、裂谷热病毒、脊髓灰质炎病毒和甲型流感病毒)的相互作用,并将分泌自噬与其他细胞外囊泡释放途径进行了比较。最后,我们强调了需要并重视更彻底的方法来研究这些途径的潜在机制,以更好地推进我们对疾病进展的理解。