Abstract
Autophagy is an essential vacuolar process of the cell, leading to lysosomal degradation and recycling of proteins and organelles, which is extremely important in maintaining homeostasis. Multiple roles have been now associated with autophagy, in particular a pro-survival role in nutrient starvation or in stressful environments, a role in life span extension, in development, or in innate and adaptive immunity. This cellular process can also take over microorganisms or viral proteins inside autophagosomes and degrade them directly in autolysosomes and is then called xenophagy and virophagy, respectively. Several Herpesviruses have developed strategies to escape this degradation, by expression of specific anti-autophagic proteins. However, we are increasingly discovering that Herpesviruses hijack autophagy, rather than just fight it. This beneficial effect is obvious since inhibition of autophagy will lead to decreased viral titers for human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) or Varicella-Zoster virus (VZV), for example. Conversely, autophagy stimulation will improve viral multiplication. The autophagic machinery can be used in whole or in part, and can optimize viral propagation or persistence. Some viruses block maturation of autophagosomes to avoid the degradation step, then autophagosomal membranes are used to contribute to the envelopment and/or the egress of viral particles. On the other hand, VZV stimulates the whole process of autophagy to subvert it in order to use vesicles containing ATG (autophagy-related) proteins and resembling amphisomes for their transport in the cytoplasm. During latency, autophagy can also be activated by latent proteins encoded by different oncogenic Herpesviruses to promote cell survival and achieve long term viral persistence in vivo. Finally, reactivation of gammaherpesvirus Murid Herpesvirus 68 (MHV68) in mice appears to be positively modulated by autophagy, in order to control the level of inflammation. Therefore, Herpesviruses appear to behave more like thieves than fugitives.
Highlights
Autophagy allows the cell to discard different cell components, from macromolecules to Autophagy allows discovered the cell tomore discard different cell components, from macromolecules organelles. than 50 years ago—the word “autophagy”was invented by to organelles. discovered than 50 years are ago—the word “autophagy”invented the Belgian biochemistChristian more de Duve in 1963—we still in the process of learningwas about the by the Belgianresources biochemist ChristianDuvemechanism in 1963—we still to in function, the process of learning about incredible of this essentialde cellular [16]. areIn order autophagy requires a conserved and complex made ofmechanismATG proteins, initially discovered the incredible resources of thismachinery, essential cellular [16]
Reactivation of gammaherpesvirus Murid Herpesvirus 68 (MHV68) in mice appears to be positively modulated by autophagy, in order to control the level of inflammation
Evidence accumulated undoubtedly demonstrates that autophagy can be beneficial to several Herpesviruses during lytic cycle and latency as well as reactivation (Table 1)
Summary
Herpesviruses were originally classified into a single family, but since 2009 they are grouped into the new order Herpesvirales and organized into three families [1]. The Alphaherpesvirinae subfamily is defined on the basis of a variable host range, relatively short reproductive cycle resulting in rapid destruction of infected cells, and the establishment of latent infections primarily in sensory ganglia. Murid Herpesvirus 68 (MHV68), and the Lymphocryptovirus genus, which includes Epstein-Barr virus (EBV) and related primate viruses They are mainly hosted by primates and latency is ordinarily established in lymphoid tissues. Un-enveloped capsids are released into the cytoplasm and acquire tegument and final envelope by budding into specialized vesicles containing the viral glycoproteins that will decorate the surface of mature virions. A role for autophagic membranes in envelopment formed, virions are translocated to the cell surface within small vesicles using exocytosis machinery and release of virions has been proposed for some herpesviruses. To the cell surface within small vesicles using exocytosis machinery and released from the cells
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