Hepatitis E Virus: How It Escapes Host Innate Immunity

Lhomme, Sébastien; Migueres, Marion; Abravanel, Florence; Marion, Olivier; Kamar, Nassim; Izopet, Jacques

doi:10.3390/vaccines8030422

Cited by 13 publications

(13 citation statements)

References 102 publications

(140 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At the same time, Lhomme et al. described the different immune escape strategies to neutralize the innate immunity of the hepatitis E virus ( 70 ). Vossen et al.…”

Section: Viral Evolution Viral Variants and Immune Escape: Overviewmentioning

confidence: 99%

See 1 more Smart Citation

A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations

et al. 2022

View full text Add to dashboard Cite

The infective SARS-CoV-2 is more prone to immune escape. Presently, the significant variants of SARS-CoV-2 are emerging in due course of time with substantial mutations, having the immune escape property. Simultaneously, the vaccination drive against this virus is in progress worldwide. However, vaccine evasion has been noted by some of the newly emerging variants. Our review provides an overview of the emerging variants’ immune escape and vaccine escape ability. We have illustrated a broad view related to viral evolution, variants, and immune escape ability. Subsequently, different immune escape approaches of SARS-CoV-2 have been discussed. Different innate immune escape strategies adopted by the SARS-CoV-2 has been discussed like, IFN-I production dysregulation, cytokines related immune escape, immune escape associated with dendritic cell function and macrophages, natural killer cells and neutrophils related immune escape, PRRs associated immune evasion, and NLRP3 inflammasome associated immune evasion. Simultaneously we have discussed the significant mutations related to emerging variants and immune escape, such as mutations in the RBD region (N439K, L452R, E484K, N501Y, K444R) and other parts (D614G, P681R) of the S-glycoprotein. Mutations in other locations such as NSP1, NSP3, NSP6, ORF3, and ORF8 have also been discussed. Finally, we have illustrated the emerging variants’ partial vaccine (BioNTech/Pfizer mRNA/Oxford-AstraZeneca/BBIBP-CorV/ZF2001/Moderna mRNA/Johnson & Johnson vaccine) escape ability. This review will help gain in-depth knowledge related to immune escape, antibody escape, and partial vaccine escape ability of the virus and assist in controlling the current pandemic and prepare for the next.

show abstract

“…At the same time, Lhomme et al. described the different immune escape strategies to neutralize the innate immunity of the hepatitis E virus ( 70 ). Vossen et al.…”

Section: Viral Evolution Viral Variants and Immune Escape: Overviewmentioning

confidence: 99%

“…Thimme et al described the different immune escape approaches of the hepatitis C virus (69). At the same time, Lhomme et al described the different immune escape strategies to neutralize the innate immunity of the hepatitis E virus (70). Vossen et al represented the immune evasion of virus in the light of viral evolution.…”

Section: Introductionmentioning

confidence: 99%

A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Moreover, a recent report showed that SARS-CoV-2 RNAs are capped at the 5' end and escape recognition from PRRs (Encinar and Menendez, 2020). Viral mechanisms of escaping from PRRs' recognition have been reviewed elsewhere (Weber et al, 2006;Abe et al, 2007;Bowie and Unterholzner, 2008;Chan and Gack, 2016;Qi et al, 2017;Chiang et al, 2018;Verrier et al, 2018;Encinar and Menendez, 2020;Kikkert, 2020;Lhomme et al, 2020;Liu et al, 2020;Zhu and Zheng, 2020).…”

Section: Escaping From the Recognition From Prrsmentioning

confidence: 99%

Acute Infection of Viral Pathogens and Their Innate Immune Escape

et al. 2021

View full text Add to dashboard Cite

Viral infections can cause rampant disease in human beings, ranging from mild to acute, that can often be fatal unless resolved. An acute viral infection is characterized by sudden or rapid onset of disease, which can be resolved quickly by robust innate immune responses exerted by the host or, instead, may kill the host. Immediately after viral infection, elements of innate immunity, such as physical barriers, various phagocytic cells, group of cytokines, interferons (IFNs), and IFN-stimulated genes, provide the first line of defense for viral clearance. Innate immunity not only plays a critical role in rapid viral clearance but can also lead to disease progression through immune-mediated host tissue injury. Although elements of antiviral innate immunity are armed to counter the viral invasion, viruses have evolved various strategies to escape host immune surveillance to establish successful infections. Understanding complex mechanisms underlying the interaction between viruses and host’s innate immune system would help develop rational treatment strategies for acute viral infectious diseases. In this review, we discuss the pathogenesis of acute infections caused by viral pathogens and highlight broad immune escape strategies exhibited by viruses.

show abstract

“…This hypothesis was partially evidenced by the fact that ORF3 protein was dispensable for in vitro replication of HEV-RNA[ 59 ]. However, subsequent research studies demonstrated that HEV-ORF3-associated putative interference mechanisms acted on multiple host cell signaling pathways, such as those involved in host innate immunity[ 2 , 68 , 69 ], indicating that HEV-ORF3 activities ultimately promote viral replication and pathogenesis.…”

Section: Regulation Of Host Innate Immunity and Signaling By Hev-orf3 Proteinmentioning

confidence: 99%

Open reading frame 3 protein of hepatitis E virus: Multi-function protein with endless potential

Yang¹,

Nan²

2021

WJG

View full text Add to dashboard Cite

Hepatitis E virus (HEV), a fecal-orally transmitted foodborne viral pathogen, causes acute hepatitis in humans and is responsible for hepatitis E outbreaks worldwide. Since the identification of HEV as a zoonotic agent, this virus has been isolated from a variety of hosts with an ever-expanding host range. HEV-open reading frame (ORF) 3, the smallest ORF in HEV genomes, initially had been perceived as an unremarkable HEV accessory protein. However, as novel HEV-ORF3 function has been discovered that is related to the existence of a putative third virion structural form, referred to as “quasi-enveloped” HEV particles, HEV is challenging the conventional virion structure-based classification scheme, which assigns all viruses to two groups, “enveloped” or “non-enveloped”. In this review, we systematically describe recent progress that has identified multiple pathogenic roles of HEV-ORF3, including roles in HEV virion release, biogenesis of quasi-enveloped virus, regulation of the host innate immune response, and interference with host signaling pathways. In addition, implications of HEV-ORF3-associated quasi-enveloped virions are discussed to guide future development of improved vaccines against zoonotic HEV infection.

show abstract

Hepatitis E Virus: How It Escapes Host Innate Immunity

Cited by 13 publications

References 102 publications

A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations

A Detailed Overview of Immune Escape, Antibody Escape, Partial Vaccine Escape of SARS-CoV-2 and Their Emerging Variants With Escape Mutations

Acute Infection of Viral Pathogens and Their Innate Immune Escape

Open reading frame 3 protein of hepatitis E virus: Multi-function protein with endless potential

Contact Info

Product

Resources

About