Manipulation of autophagy by (+) RNA viruses

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Abstract

Autophagy is an evolutionarily conserved process central to host metabolism. Among its major functions are conservation of energy during starvation, recycling organelles, and turnover of long-lived proteins. Besides, autophagy plays a critical role in removing intracellular pathogens and very likely represents a primordial intrinsic cellular defence mechanism. More recent findings indicate that it has not only retained its ability to degrade intracellular pathogens, but also functions to augment and fine tune antiviral immune responses. Interestingly, viruses have also co-evolved strategies to manipulate this pathway and use it to their advantage. Particularly intriguing is infection-dependent activation of autophagy with positive stranded (+)RNA virus infections, which benefit from the pathway without succumbing to lysosomal degradation. In this review we summarise recent data on viral manipulation of autophagy, with a particular emphasis on +RNA viruses and highlight key unanswered questions in the field that we believe merit further attention.

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Most cited references 71

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Autophagy in cell death: an innocent convict?

Junying Yuan, Beth Levine (2005)

The visualization of autophagosomes in dying cells has led to the belief that autophagy is a nonapoptotic form of programmed cell death. This concept has now been evaluated using cells and organisms deficient in autophagy genes. Most evidence indicates that, at least in cells with intact apoptotic machinery, autophagy is primarily a pro-survival rather than a pro-death mechanism. This review summarizes the evidence linking autophagy to cell survival and cell death, the complex interplay between autophagy and apoptosis pathways, and the role of autophagy-dependent survival and death pathways in clinical diseases.

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Modification of intracellular membrane structures for virus replication

Sven Miller, Jacomine Krijnse-Locker (2008)

Key Points Plus-stranded RNA viruses induce large membrane structures that might support the replication of their genomes. Similarly, cytoplasmic replication of poxviruses (large DNA viruses) occurs in associated membranes. These membranes originate from the endoplasmic reticulum (ER) or endosomes. Membrane vesicles that support viral replication are induced by a number of RNA viruses. Similarly, the poxvirus replication site is surrounded by a double-membraned cisterna that is derived from the ER. Analogies to autophagy have been proposed since the finding that autophagy cellular processes involve the formation of double-membrane vesicles. However, molecular evidence to support this hypothesis is lacking. Membrane association of the viral replication complex is mediated by the presence of one or more viral proteins that contain sequences which associate with, or integrate into, membranes. Replication-competent membranes might contain viral or cellular proteins that contain amphipathic helices, which could mediate the membrane bending that is required to form spherical vesicles. Whereas poxvirus DNA replication occurs inside the ER-enclosed site, for most RNA viruses the topology of replication is not clear. Preliminary results for some RNA viruses suggest that their replication could also occur inside double-membrane vesicles. We speculate that cytoplasmic replication might occur inside sites that are 'enwrapped' by an ER-derived cisterna, and that these cisternae are open to the cytoplasm. Thus, RNA and DNA viruses could use a common mechanism for replication that involves membrane wrapping by cellular cisternal membranes. We propose that three-dimensional analyses using high-resolution electron-microscopy techniques could be useful for addressing this issue. High-throughput small-interfering-RNA screens should also shed light on molecular requirements for virus-induced membrane modifications.

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Lysosomes and autophagy in cell death control.

Guido Kroemer, Marja Jäättelä (2005)

Lysosomal hydrolases participate in the digestion of endocytosed and autophagocytosed material inside the lysosomal/autolysosomal compartment in acute cell death when released into the cytosol and in cancer progression following their release into the extracellular space. Lysosomal alterations are common in cancer cells. The increased expression and altered trafficking of lysosomal enzymes participates in tissue invasion, angiogenesis and sensitization to the lysosomal death pathway. But lysosomal heat-shock protein 70 locally prevents lysosomal-membrane permeabilization. Similarly, alterations in the autophagic compartment are linked to carcinogenesis and resistance to chemotherapy. Targeting these pathways might constitute a novel approach to cancer therapy.

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Author and article information

Contributors

Sumana Sanyal

Journal

Journal ID (nlm-ta): Semin Cell Dev Biol

Journal ID (iso-abbrev): Semin. Cell Dev. Biol

Title: Seminars in Cell & Developmental Biology

Publisher: Academic Press

ISSN (Print): 1084-9521

ISSN (Electronic): 1096-3634

Publication date PMC-release: 8 August 2019

Publication date (Electronic): 8 August 2019

Affiliations

[a ]HKU-Pasteur Research Pole, School of Public Health, University of Hong Kong, Hong Kong

[b ]School of Biomedical Sciences, LKS Faculty of Medicine, University of Hong Kong, Hong Kong

Author notes

[* ]Corresponding author at: HKU-Pasteur Research Pole, School of Public Health, University of Hong Kong, Hong Kong. sanyal@ 123456hku.hk

Article

Publisher ID: S1084-9521(18)30222-2

DOI: 10.1016/j.semcdb.2019.07.013

PMC ID: 7102625

PubMed ID: 31382014

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Manipulation of autophagy by (+) RNA viruses

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Abstract

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RNA drug delivery

Most cited references 71

Autophagy in cell death: an innocent convict?

Modification of intracellular membrane structures for virus replication

Lysosomes and autophagy in cell death control.

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Contributors

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