MDA5 against enteric viruses through induction of interferon-like response partially via the JAK-STAT cascade

Li, Yang; Yu, Peifa; Qu, Changbo; Li, Pengfei; Li, Yunlong; Ma, Zhiyong; Wang, Wenshi; Man, Robert A. de; Peppelenbosch, Maikel P.

doi:10.1016/j.antiviral.2020.104743

Cited by 17 publications

(19 citation statements)

References 33 publications

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“…In hepatoma cell lines HepG2/C3A and Huh7:S10-3 transfected with HEV subgenomic RNA, Mda5 expression was higher after 24 h posttransfection and it was associated with viral RNA replication as Mda5 expression was comparatively less in cells transfected with replication-deficient RNA [39]. Recently, Li et al (2020) demonstrated the role of Mda5 in inhibiting HEV replication in both HEV infectious and subgenomic replicon models [44]. The overexpression of Mda5 mediated its antiviral action by inducing a wide range of antiviral ISGs independent of interferon production through partial activation of JAK-STAT signaling [44].…”

Section: Hev Sensing By Rlrsmentioning

confidence: 99%

“…Recently, Li et al (2020) demonstrated the role of Mda5 in inhibiting HEV replication in both HEV infectious and subgenomic replicon models [44]. The overexpression of Mda5 mediated its antiviral action by inducing a wide range of antiviral ISGs independent of interferon production through partial activation of JAK-STAT signaling [44].…”

Section: Hev Sensing By Rlrsmentioning

confidence: 99%

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Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Devhare

Madiyal

Mukhopadhyay

et al. 2021

IJMS

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Hepatitis E virus (HEV) usually causes self-limiting acute hepatitis, but the disease can become chronic in immunocompromised individuals. HEV infection in pregnant women is reported to cause up to 30% mortality, especially in the third trimester. Additionally, extrahepatic manifestations like neuronal and renal diseases and pancreatitis are also reported during the course of HEV infection. The mechanism of HEV pathogenesis remains poorly understood. Innate immunity is the first line of defense triggered within minutes to hours after the first pathogenic insult. Growing evidence based on reverse genetics systems, in vitro cell culture models, and representative studies in animal models including non-human primates, has implicated the role of the host’s innate immune response during HEV infection. HEV persists in presence of interferons (IFNs) plausibly by evading cellular antiviral defense. This review summarizes our current understanding of recognizing HEV-associated molecular patterns by host cell Pattern Recognition Receptors (PRRs) in eliciting innate immune response during HEV infection as well as mechanisms of virus-mediated immune evasion.

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Section: Hev Sensing By Rlrsmentioning

confidence: 99%

Section: Hev Sensing By Rlrsmentioning

confidence: 99%

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Devhare

Madiyal

Mukhopadhyay

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…MAVS depletion exerted a more severe IFNβ antagonizing effect in RV-infected settings than when RIG1 or MDA5 was depleted alone, suggesting MAVS to act as a common adaptor downstream of both RIG1 and MDA5 [103,104]. Nevertheless, MDA5 overexpression significantly attenuated RV replication through upregulation of many ISGs possibly bypassing the involvement of JAK-STAT pathway [113]. Unlike the initial PAMP sensing machinery, many of the downstream effectors involved in mounting initial IFN response are targeted strategically by RVs, particularly by NSP1 (the IFN antagonist of RV) [114,115].…”

Section: Host Pattern Recognition Receptors and Ifn-signaling Cascadementioning

confidence: 96%

Treading a HOSTile path: Mapping the dynamic landscape of host cell–rotavirus interactions to explore novel host-directed curative dimensions

et al. 2021

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Viruses are intracellular pathogens and are dependent on host cellular resources to carry out their cycles of perpetuation. Obtaining an integrative view of host–virus interaction is of utmost importance to understand the complex and dynamic interplay between viral components and host machineries. Besides its obvious scholarly significance, a comprehensive host–virus interaction profile also provides a platform where from host determinants of pro-viral and antiviral importance can be identified and further be subjected to therapeutic intervention. Therefore, adjunct to conventional methods of prophylactic vaccination and virus-directed antivirals, this host-targeted antiviral approach holds promising therapeutic potential. In this review, we present a comprehensive landscape of host cellular reprogramming in response to infection with rotavirus (RV) which causes profuse watery diarrhea in neonates and infants. In addition, an emphasis is given on how host determinants are either usurped or subverted by RV in course of infection and how therapeutic manipulation of specific host factors can effectively modulate the RV life cycle.

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“…IRF1 and MDA5 delivered by the same system also had anti-HEV activity 72 h post-transduction [ 53 ]. MDA5 overexpression in Huh7 cells also inhibited HEV3–Kernow replication by triggering an antiviral, IFN-like response [ 54 ]. Others have shown that IRF1 has antiviral activity in Huh7 cells transfected with the HEV1–Sar55 or the HEV3–Kernow replicon, as well as in Huh7 cells infected with HEV3–Kernow [ 55 ].…”

Section: Hev Rna Sensing By Infected Cellsmentioning

confidence: 99%

Hepatitis E Virus: How It Escapes Host Innate Immunity

et al. 2020

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Hepatitis E virus (HEV) is a leading cause of viral hepatitis in the world. It is usually responsible for acute hepatitis, but can lead to a chronic infection in immunocompromised patients. The host’s innate immune response is the first line of defense against a virus infection; there is growing evidence that HEV RNA is recognized by toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs), leading to interferon (IFN) production. The IFNs activate interferon-stimulated genes (ISGs) to limit HEV replication and spread. HEV has developed strategies to counteract this antiviral response, by limiting IFN induction and signaling. This review summarizes the advances in our knowledge of intracellular pathogen recognition, interferon and inflammatory response, and the role of virus protein in immune evasion.

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MDA5 against enteric viruses through induction of interferon-like response partially via the JAK-STAT cascade

Cited by 17 publications

References 33 publications

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Interplay between Hepatitis E Virus and Host Cell Pattern Recognition Receptors

Treading a HOSTile path: Mapping the dynamic landscape of host cell–rotavirus interactions to explore novel host-directed curative dimensions

Hepatitis E Virus: How It Escapes Host Innate Immunity

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