Inducible GBP5 Mediates the Antiviral Response via Interferon-Related Pathways during Influenza A Virus Infection

Feng, Jian; Cao, Zhongying; Wang, Li; Wan, Yi; Peng, Nanfang; Wang, Qing; Chen, Xueyuan; Zhou, Yaqin; Zhu, Ying

doi:10.1159/000460294

Cited by 47 publications

(38 citation statements)

References 73 publications

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“…Results of Feng, et al . 21 revealed that GBP5 inhibited virus replication through the activation of influenza signaling and pro-inflammatory factors. IFITM3 also restricted the replication of influenza 22 .…”

Section: Discussionmentioning

confidence: 99%

Sex-specific patterns of gene expression following influenza vaccination

Wen

Guo

et al. 2018

Sci Rep

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Sex-based variations in the immune response to the influenza vaccines was reported, however, the genetic basis responsible for the sex variations in the immune response toward the influenza vaccines remains unclear. Here, the genes responsible for sex-specific responses after vaccination with trivalent inactivated influenza virus were identified. These genes were enriched in virus response pathways, especially interferon signaling. A list of genes showing different responses to the vaccine between females and males were obtained next. Our results demonstrated that females generate stronger immune responses to seasonal influenza vaccines within 24 hours than males. However, most of these genes with variability between sexes had the opposite expression levels after three days, suggesting that males retained the immune responses longer than female. To summary, our study identified genes responsible for the sex variations toward influenza vaccination. Our findings might provide insights into the development of the sex-dependent influenza vaccines.

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Section: Discussionmentioning

confidence: 99%

Sex-specific patterns of gene expression following influenza vaccination

Wen

Guo

et al. 2018

Sci Rep

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“…In this context, it would be interesting to analyze if GBP5 may contribute to its activation. In addition to inflammasome activation, GBP5 is also able to stimulate the NF-κB signaling pathway enhancing IFN expression and IFN-related effectors [279]. Thus, after activation by innate immunity, GBP5 may in return, amplify this immune response.…”

Section: Restriction Factors Shaping Immunitymentioning

confidence: 99%

Interplay between Intrinsic and Innate Immunity during HIV Infection

Bergantz

Subra

Deprez

et al. 2019

Cells

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Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed.

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“…In contrast, GTP binding, but not hydrolysis, was essential for the ability of a splice variant of human GBP3 to repress the activity of the viral polymerase complex and inhibit IAV replication [ 52 ]. A recent study also demonstrated that overexpression of human GBP5 inhibited virus replication by enhancing the expression of virus-induced IFN and IFN-related effectors [ 53 ]. These findings highlight the potential of GBPs as anti-IAV effectors although further studies are required to assess the antiviral activities of different GBP-family members, as well as their relevance in vivo.…”

Section: Restriction Factors That Interfere With Genomic Transcripmentioning

confidence: 99%

Host Cell Restriction Factors that Limit Influenza A Infection

Villalón-Letelier

Brööks

Saunders

et al. 2017

Viruses

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Viral infection of different cell types induces a unique spectrum of host defence genes, including interferon-stimulated genes (ISGs) and genes encoding other proteins with antiviral potential. Although hundreds of ISGs have been described, the vast majority have not been functionally characterised. Cellular proteins with putative antiviral activity (hereafter referred to as “restriction factors”) can target various steps in the virus life-cycle. In the context of influenza virus infection, restriction factors have been described that target virus entry, genomic replication, translation and virus release. Genome wide analyses, in combination with ectopic overexpression and/or gene silencing studies, have accelerated the identification of restriction factors that are active against influenza and other viruses, as well as providing important insights regarding mechanisms of antiviral activity. Herein, we review current knowledge regarding restriction factors that mediate anti-influenza virus activity and consider the viral countermeasures that are known to limit their impact. Moreover, we consider the strengths and limitations of experimental approaches to study restriction factors, discrepancies between in vitro and in vivo studies, and the potential to exploit restriction factors to limit disease caused by influenza and other respiratory viruses.

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Inducible GBP5 Mediates the Antiviral Response via Interferon-Related Pathways during Influenza A Virus Infection

Cited by 47 publications

References 73 publications

Sex-specific patterns of gene expression following influenza vaccination

Sex-specific patterns of gene expression following influenza vaccination

Interplay between Intrinsic and Innate Immunity during HIV Infection

Host Cell Restriction Factors that Limit Influenza A Infection

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