Distinct Contributions of Autophagy Receptors in Measles Virus Replication

Petkova, Denitsa S; Verlhac, Pauline; Rozières, Aurore; Baguet, Joël; Claviere, Mathieu; Kretz-Remy, Carole; Mahieux, Renaud; Viret, Christophe; Faure, Mathias

doi:10.3390/v9050123

Cited by 41 publications

(44 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the case of viral infection, reported that NDP52 binds to the coxsackievirus B3 viral protein VP1 and mediates VP1 ubiquitination via the K48 ubiquitin pathway. Other studies have shown that CALCOCO2 binds the nonstructural protein 2 of the Chikungunya virus to promote viral replication in humans (Judith et al, 2013), and plays a proviral role in measles viral infection (Petkova et al, 2017). In this study, our results showed that CSFV infection inhibits NDP52 expression.…”

Section: Discussionsupporting

confidence: 62%

Dual NDP52 Function in Persistent CSFV Infection

Fan

Luo

et al. 2020

Front. Microbiol.

View full text Add to dashboard Cite

Viruses have evolved many mechanisms to escape host antiviral responses. Previously, we found that classical swine fever virus (CSFV) infection induces autophagy using the autophagosome as a self-replication site, thereby evading the host immune response and promoting long-term infection. However, the underlying mechanisms used by CSFV to enter autophagosomes and the mechanism by which autophagy promotes viral replication remain unclear. We found that CSFV infection inhibited autophagy receptor nuclear dot protein 52 kDa (NDP52) expression, ubiquitination, and SUMO2-4 modification. Further analyses revealed that CSFV mediated ubiquitination and SUMOylation of NDP52 via Pten-induced kinase 1 (PINK1)-Parkin. Moreover, NDP52 inhibition also inhibited CSFV replication and the induction of mitophagy marker proteins expression. Inhibition of NDP52 reduced CD63 expression and binding to CSFV E2 protein, which has an essential role in persistent CSFV infection. As NDP52 has a close relationship with the NF-κB innate immunity pathway and plays an important role in the antiviral response, we investigated whether NDP52 inhibited CSFV replication through the release of immune factors and antivirus signals. Our results showed that inhibiting NDP52 boosted interferon and TNF release and promoted NF-κB pathway activation. In summary, we found that NDP52 inhibition not only reduces CSFV binding and entry into autophagic vesicles, but also inhibits CSFV replication by active NF-κB antiviral immune pathways. Our data reveal a novel mechanism by which NDP52, an autophagy receptor, mediates CSFV infection, and provide new avenues for the development of antiviral strategies.

show abstract

Section: Discussionsupporting

confidence: 62%

Dual NDP52 Function in Persistent CSFV Infection

Fan

Luo

et al. 2020

Front. Microbiol.

View full text Add to dashboard Cite

show abstract

“…5.1, Step 2). This pathway is only sensitive to vaccinal/attenuated strains that utilize CD46 to infect cells [59,91,96,106,112,118]. In fact, MeV also activates autophagy by targeting an autophagy associated protein, named as immunity-associated GTPase family M (IRGM) [45,46,107].…”

mentioning

confidence: 99%

Autophagy and Viral Infection

Mao

Lin

et al. 2019

Advances in Experimental Medicine and Biology

114

View full text Add to dashboard Cite

Autophagy is an intracellular recycling process that maintains cellular homeostasis by orchestrating immunity upon viral infection. Following viral infection, autophagy is often initiated to curtail infection by delivering viral particles for lysosomal degradation and further integrating with innate pattern recognition receptor signaling to induce interferon (IFN)-mediated viral clearance. However, some viruses have evolved anti-autophagy strategies to escape host immunity and to promote viral replication. In this chapter, we illustrate how autophagy prevents viral infection to generate an optimal anti-viral milieu, and then concentrate on how viruses subvert and hijack the autophagic process to evade immunosurveillance, thereby facilitating viral replication and pathogenesis. Understanding the interplays between autophagy and viral infection is anticipated to guide the development of effective anti-viral therapeutics to fight against infectious diseases.

show abstract

“…Measles virus (MeV) is an enveloped virus with a negative-stranded RNA genome [87], which can induce autophagy during viral infection, thereby promoting its replication [88,89]. Studies have shown that NDP52 plays an important role in regulating viral replication by binding to MeV-C and MeV-V proteins in MeV-infected cells [90]. Furthermore, the inhibition of NDP52 significantly reduces MeV replication not through the entry of the virus, but the maturation of autophagosome.…”

Section: The Role and Mechanism Of Ndp52 In Viral Infectionsmentioning

confidence: 99%

The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections

Fan

Zhu

et al. 2020

IJMS

View full text Add to dashboard Cite

Autophagy is a general protective mechanism for maintaining homeostasis in eukaryotic cells, regulating cellular metabolism, and promoting cell survival by degrading and recycling cellular components under stress conditions. The degradation pathway that is mediated by autophagy receptors is called selective autophagy, also named as xenophagy. Autophagy receptor NDP52 acts as a ‘bridge’ between autophagy and the ubiquitin-proteasome system, and it also plays an important role in the process of selective autophagy. Pathogenic microbial infections cause various diseases in both humans and animals, posing a great threat to public health. Increasing evidence has revealed that autophagy and autophagy receptors are involved in the life cycle of pathogenic microbial infections. The interaction between autophagy receptor and pathogenic microorganism not only affects the replication of these microorganisms in the host cell, but it also affects the host’s immune system. This review aims to discuss the effects of autophagy on pathogenic microbial infection and replication, and summarizes the mechanisms by which autophagy receptors interact with microorganisms. While considering the role of autophagy receptors in microbial infection, NDP52 might be a potential target for developing effective therapies to treat pathogenic microbial infections.

show abstract

Distinct Contributions of Autophagy Receptors in Measles Virus Replication

Cited by 41 publications

References 35 publications

Dual NDP52 Function in Persistent CSFV Infection

Dual NDP52 Function in Persistent CSFV Infection

Autophagy and Viral Infection

The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections

Contact Info

Product

Resources

About