Autophagy in antiviral innate immunity

Richetta, Clémence; Faure, Mathias

doi:10.1111/cmi.12043

Cited by 109 publications

(93 citation statements)

References 47 publications

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“…Autophagy and/or autophagy-related genes have both antiviral and proviral effects on the life cycles and pathogenesis of many different viruses (82). As we have shown for HIV (32), autophagy can target incoming virions or viral components (80) for lysosomal degradation.…”

Section: Discussionmentioning

confidence: 99%

HIV-Infected Dendritic Cells Present Endogenous MHC Class II–Restricted Antigens to HIV-Specific CD4+ T Cells

Coulon

Richetta

Rouers

et al. 2016

The Journal of Immunology

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It is widely assumed that CD4+ T cells recognize antigenic peptides (epitopes) derived solely from incoming, exogenous, viral particles or proteins. However, alternative sources of MHC class II (MHC-II)–restricted Ags have been described, in particular epitopes derived from newly synthesized proteins (so-called endogenous). In this study, we show that HIV-infected dendritic cells (DC) present MHC-II–restricted endogenous viral Ags to HIV-specific (HS) CD4+ T cells. This endogenous pathway functions independently of the exogenous route for HIV Ag presentation and offers a distinct possibility for the immune system to activate HS CD4+ T cells. We examined the implication of autophagy, which plays a crucial role in endogenous viral Ag presentation and thymic selection of CD4+ T cells, in HIV endogenous presentation. We show that infected DC do not use autophagy to process MHC-II–restricted HIV Ags. This is unlikely to correspond to a viral escape from autophagic degradation, as infecting DC with Nef- or Env-deficient HIV strains did not impact HS T cell activation. However, we demonstrate that, in DC, specific targeting of HIV Ags to autophagosomes using a microtubule-associated protein L chain 3 (LC3) fusion protein effectively enhances and broadens HS CD4+ T cell responses, thus favoring an endogenous MHC-II–restricted presentation. In summary, in DC, multiple endogenous presentation pathways lead to the activation of HS CD4+ T cell responses. These findings will help in designing novel strategies to activate HS CD4+ T cells that are required for CTL activation/maintenance and B cell maturation.

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Section: Discussionmentioning

confidence: 99%

HIV-Infected Dendritic Cells Present Endogenous MHC Class II–Restricted Antigens to HIV-Specific CD4+ T Cells

Coulon

Richetta

Rouers

et al. 2016

The Journal of Immunology

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“…Autophagy has a role in cellular homeostasis and is also an innate immune mechanism that can selectively target intracellular pathogens and cytosolic proteins for enzymatic degradation (He & Klionsky, 2009;Richetta & Faure, 2013;Sumpter & Levine, 2010). Protein kinase R (PKR) is a vertebrate interferon stimulated gene that can trigger autophagy upon dsRNA binding through a pathway involving eIF2a (reviewed by Richetta & Faure, 2013). Vertebrate cells can utilize this PKR and eIF2a-dependent autophagy pathway to degrade both herpes simplex virus type 1 (HSV-1) virions and HSV-1 proteins (Talló czy et al, 2006).…”

Section: Programmed Cell Death (Pcd)mentioning

confidence: 99%

“…Human cytomegalovirus (HCMV) and HSV-1 induced autophagy in human fibroblasts and this response was retained when cells were infected with UV-irradiated HCMV (McFarlane et al, 2011). Other pathogen sensors (such as TLR3, TLR4, TLR7, TLR8 and NOD2) are also known to induce autophagy upon binding with their specific ligand, via a MyD88 independent pathway (reviewed by Richetta & Faure, 2013). Autophagy is also an antiviral mechanism utilized by arthropods (Nakamoto et al, 2012).…”

Section: Programmed Cell Death (Pcd)mentioning

confidence: 99%

Antiviral immunity in marine molluscs

Green

Raftos

Speck

et al. 2015

Journal of General Virology

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Marine molluscs, like all living organisms, are constantly exposed to viruses and have evolved efficient antiviral defences. We review here recent developments in molluscan antiviral immunity against viruses belonging to the order Herpesvirales. Emerging results suggest an interferon-like response and autophagy are involved in the antiviral defence of bivalves to viral infection. Multifunctional plasma proteins from gastropods and bivalves have been identified to have broadspectrum antiviral activity against mammalian viruses. The antiviral defences present in molluscs can be enhanced by genetic selection, as shown by the presence of oyster strains specifically resistant to ostreid herpesvirus type 1. Whether varying amounts or different isoforms of these antiviral plasma proteins contributes to genetic resistance is worthy of further research. Other evolutionarily conserved antiviral mechanisms, such as RNA interference and apoptosis, still need further characterization.

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“…In addition, autophagy emerges as a component of innate immunity as it can destroy infectious viruses or viral components essential for viral replication or assembly, a process referred to as virophagy, linking virus detection to antiviral innate immune signals or participating in the regulation of immune and inflammatory cell response [107,108]. In this circumstance, HDAC6 facilitates aggresome formation and autophagic degradation for the clearance of intracellular invasive viruses or viral proteins.…”

Section: Controlling Antiviral Immune Responsesmentioning

confidence: 99%

Cellular defence or viral assist: the dilemma of HDAC6

Zheng

Jiang

et al. 2017

Journal of General Virology

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Histone deacetylase 6 (HDAC6) is a unique cytoplasmic deacetylase that regulates various important biological processes by preventing protein aggregation and deacetylating different non-histone substrates including tubulin, heat shock protein 90, cortactin, retinoic acid inducible gene I and b-catenin. Growing evidence has indicated a dual role for HDAC6 in viral infection and pathogenesis: HDAC6 may represent a host defence mechanism against viral infection by modulating microtubule acetylation, triggering antiviral immune response and stimulating protective autophagy, or it may be hijacked by the virus to enhance proinflammatory response. In this review, we will highlight current data illustrating the complexity and importance of HDAC6 in viral pathogenesis. We will summarize the structure and functional specificity of HDAC6, and its deacetylaseand ubiquitin-dependent activity in key cellular events in response to virus infection. We will also discuss how HDAC6 exerts its direct or indirect histone modification ability in viral lytic-latency switch.

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Autophagy in antiviral innate immunity

Cited by 109 publications

References 47 publications

HIV-Infected Dendritic Cells Present Endogenous MHC Class II–Restricted Antigens to HIV-Specific CD4+ T Cells

HIV-Infected Dendritic Cells Present Endogenous MHC Class II–Restricted Antigens to HIV-Specific CD4+ T Cells

Antiviral immunity in marine molluscs

Cellular defence or viral assist: the dilemma of HDAC6

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