The roles of apoptosis, autophagy and unfolded protein response in arbovirus, influenza virus, and HIV infections

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ABSTRACT

Virus infection induces different cellular responses in infected cells. These include cellular stress responses like autophagy and unfolded protein response (UPR). Both autophagy and UPR are connected to programed cell death I (apoptosis) in chronic stress conditions to regulate cellular homeostasis via Bcl2 family proteins, CHOP and Beclin-1. In this review article we first briefly discuss arboviruses, influenza virus, and HIV and then describe the concepts of apoptosis, autophagy, and UPR. Finally, we focus upon how apoptosis, autophagy, and UPR are involved in the regulation of cellular responses to arboviruses, influenza virus and HIV infections.

Abbreviation: AIDS: Acquired Immunodeficiency Syndrome; ATF6: Activating Transcription Factor 6; ATG6: Autophagy-specific Gene 6; BAG3: BCL Associated Athanogene 3; Bak: BCL-2-Anatagonist/Killer1; Bax; BCL-2: Associated X protein; Bcl-2: B cell Lymphoma 2x; BiP: Chaperon immunoglobulin heavy chain binding Protein; CARD: Caspase Recruitment Domain; cART: combination Antiretroviral Therapy; CCR5: C-C Chemokine Receptor type 5; CD4: Cluster of Differentiation 4; CHOP: C/EBP homologous protein; CXCR4: C-X-C Chemokine Receptor Type 4; Cyto c: Cytochrome C; DCs: Dendritic Cells; EDEM1: ER-degradation enhancing-a-mannosidase-like protein 1; ENV: Envelope; ER: Endoplasmic Reticulum; FasR: Fas Receptor;G2: Gap 2; G2/M: Gap2/Mitosis; GFAP: Glial Fibrillary Acidic Protein; GP120: Glycoprotein120; GP41: Glycoprotein41; HAND: HIV Associated Neurodegenerative Disease; HEK: Human Embryonic Kidney; HeLa: Human Cervical Epithelial Carcinoma; HIV: Human Immunodeficiency Virus; IPS-1: IFN-β promoter stimulator 1; IRE-1: Inositol Requiring Enzyme 1; IRGM: Immunity Related GTPase Family M protein; LAMP2A: Lysosome Associated Membrane Protein 2A; LC3: Microtubule Associated Light Chain 3; MDA5: Melanoma Differentiation Associated gene 5; MEF: Mouse Embryonic Fibroblast; MMP: Mitochondrial Membrane Permeabilization; Nef: Negative Regulatory Factor; OASIS: Old Astrocyte Specifically Induced Substrate; PAMP: Pathogen-Associated Molecular Pattern; PERK: Pancreatic Endoplasmic Reticulum Kinase; PRR: Pattern Recognition Receptor; Puma: P53 Upregulated Modulator of Apoptosis; RIG-I: Retinoic acid-Inducible Gene-I; Tat: Transactivator Protein of HIV; TLR: Toll-like receptor; ULK1: Unc51 Like Autophagy Activating Kinase 1; UPR: Unfolded Protein Response; Vpr: Viral Protein Regulatory; XBP1: X-Box Binding Protein 1

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Most cited references 237

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Guidelines for the use and interpretation of assays for monitoring autophagy.

C N Estevez, S M Lee, Qing Zhong … (2012)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

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Dynamics and diversity in autophagy mechanisms: lessons from yeast.

Hitoshi Nakatogawa, Kuninori Suzuki, Yoshiaki Kamada … (2009)

Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy.

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Nix is a selective autophagy receptor for mitochondrial clearance.

Ivana Novak, Vladimir Kirkin, David G McEwan … (2010)

Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy mediates selective removal of protein aggregates, organelles and microbes in cells. Yet, the specificity in targeting a particular substrate to the autophagy pathway remains poorly understood. Here, we show that the mitochondrial protein Nix is a selective autophagy receptor by binding to LC3/GABARAP proteins, ubiquitin-like modifiers that are required for the growth of autophagosomal membranes. In cultured cells, Nix recruits GABARAP-L1 to damaged mitochondria through its amino-terminal LC3-interacting region. Furthermore, ablation of the Nix:LC3/GABARAP interaction retards mitochondrial clearance in maturing murine reticulocytes. Thus, Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation.

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Author and article information

Journal

Journal ID (nlm-ta): Virulence

Journal ID (iso-abbrev): Virulence

Journal ID (publisher-id): KVIR

Journal ID (publisher-id): kvir20

Title: Virulence

Publisher: Taylor & Francis

ISSN (Print): 2150-5594

ISSN (Electronic): 2150-5608

Publication date Collection: 2019

Publication date (Electronic): 30 April 2019

Publication date PMC-release: 30 April 2019

Volume: 10

Issue: 1

Pages: 376-413

Affiliations

[a ]Influenza and Respiratory Viruses Department, Past eur Institute of IRAN , Tehran, Iran

[b ]Department of Internal Medicine, University of Manitoba , Winnipeg, MB, Canada

[c ]Department of Human Anatomy & Cell Science, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba , Winnipeg, MB, Canada

[d ]Children‘s Hospital Research Institute of Manitoba , Winnipeg, MB, Canada

[e ]Research Institute of Oncology and Hematology, CancerCare Manitoba, University of Manitoba , Winnipeg, Canada

[f ]Department of Medical Microbiology, Assiniboine Community College, School of Health and Human Services and Continuing Education , Winnipeg, MB, Canada

[g ]Department of Biology, Islamic Azad University , Mashhad, Iran

[h ]Department of Clinical Biochemistry, Zahedan University of Medical Sciences , Zahedan, Iran

[i ]Department of Medical Microbiology and Infectious Diseases, University of Manitoba , Winnipeg, MB, Canada

[j ]Manitoba Centre for Proteomics and Systems Biology, University of Manitoba , Winnipeg, MB, Canada

[k ]Health Policy Research Centre, Shiraz Medical University of Medical Science , Shiraz, Iran

Author notes

CONTACT Kevin M. Coombs Kevin.Coombs@ 123456umanitoba.ca

Saeid Ghavami Saeid.Ghavami@ 123456umanitoba.ca

Author information

Parvaneh Mehrbod http://orcid.org/0000-0002-8391-9228

Javad Alizadeh http://orcid.org/0000-0001-9082-3083

Mohammad Hashemi http://orcid.org/0000-0002-6074-7101

Saeid Ghavami http://orcid.org/0000-0001-5948-508X

Article

Publisher ID: 1605803

DOI: 10.1080/21505594.2019.1605803

PMC ID: 6527025

PubMed ID: 30966844

SO-VID: 27b8192d-5e73-4650-a65a-eff0ea0628e0

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 14 December 2018

Date revision received : 16 March 2019

Date accepted : 8 April 2019

Page count

Figures: 7, Tables: 7, References: 338, Pages: 38

Funding

Funded by: CHRIM operating grant, NIMAD operating grant and Research Manitoba New investigator award

Funded by: CHRIM operating grant and by a CIHR operating grant

SG was supported by a CHRIM operating grant, NIMAD operating grant and Research Manitoba New investigator award. KMC was supported by a CHRIM operating grant and by a CIHR operating grant. JA was supported by Canadian Lung Association PhD studentship and Research Manitoba PhD entrance scholarship.

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The roles of apoptosis, autophagy and unfolded protein response in arbovirus, influenza virus, and HIV infections

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Most cited references 237

Guidelines for the use and interpretation of assays for monitoring autophagy.

Dynamics and diversity in autophagy mechanisms: lessons from yeast.

Nix is a selective autophagy receptor for mitochondrial clearance.

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