Toll-like receptor 3 pathway restricts Marek’s disease virus infection

Zou, Haitao; Su, Ruixue; Ruan, Jing; Shao, Hongxia; Qian, Kun; Ye, Jianqiang; Qin, Aijian

doi:10.18632/oncotarget.20003

Cited by 12 publications

(12 citation statements)

References 31 publications

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“…In mice, it has been reported that the activation of TLR7 increased production of type 1 IFNs (IFNα) [54]. In chickens, type 1 IFNs produced following TLR3 ligand, dsRNA has been shown to inhibit avian viruses such as avian paramyxovirus, avian influenza virus and Marek’s disease virus [55–57]. However, we found that no significant induction of type 1 IFNs production following stimulation of avian macrophages with resiquimod.…”

Section: Discussionmentioning

confidence: 60%

Single stranded (ss)RNA-mediated antiviral response against infectious laryngotracheitis virus infection

et al. 2019

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BackgroundSingle stranded ribonucleic acid (ssRNA) binds to toll-like receptor (TLR)7 leading to recruitment of immune cells and production of pro-inflammatory cytokines, which has been shown in mammals. In chickens, synthetic ssRNA analog, resiquimod, has been shown to elicit antiviral response against infectious bursal disease virus infection. The objective of this study was to determine the innate host responses activated by the pre-hatch in ovo administration of resiquimod against infectious laryngotracheitis virus (ILTV) infection in chickens post-hatch.ResultsFirst, we observed that in ovo treatment of resiquimod at embryo day (ED) 18 increases macrophage recruitment in respiratory and gastrointestinal tissues of chicken day 1 post-hatch in addition to interleukin (IL)-1β in lungs. Second, we observed that in ovo treatment of resiquimod reduces ILTV cloacal shedding at 7 days post-infection (dpi) when challenged at day 1 post-hatch coinciding with higher macrophage recruitment. In vitro, we found that resiquimod enhances production of nitric oxide (NO) and IL-1β and not type 1 interferon (IFN) activity in avian macrophages. Although, the antiviral response against ILTV is associated with the enhanced innate immune response, it is not dependent on any of the innate immune mediators observed as has been shown in vitro using avian macrophage.ConclusionThis study provides insights into the mechanisms of antiviral response mediated by resiquimod, particularly against ILTV infection in chicken.

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Section: Discussionmentioning

confidence: 60%

Single stranded (ss)RNA-mediated antiviral response against infectious laryngotracheitis virus infection

et al. 2019

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“…This was unexpected based on previous studies using the chicken and GaHV-2 model that reported increased levels of pro-inflammatory mediators, both in vivo [29, 30, 38] and in vitro [32]. These responses probably took place within 24 h post-infection, and it is conceived that antiviral effects are linked to the early synthesis of pro-inflammatory cytokines in CEFs [26, 30]. In vivo studies have shown that as early as 3–4 days post-infection, if not earlier, various innate immune responses are detectable under normal circumstances (i.e.…”

Section: Discussionmentioning

confidence: 98%

“…This is of importance because an efficient response to infection in the early recognition of GaHV-2 has been shown to be crucial to the determination of either a positive or negative outcome [26]. Previous studies demonstrated that herpesviruses triggered innate immune signalling cascades when binding to PRRs, including TLRs, retinoic acid-inducible gene I-like receptors (RLRs), and cytosolic DNA sensors [27].…”

Section: Introductionmentioning

confidence: 99%

PFOS mediates immunomodulation in an avian cell line that can be mitigated via a virus infection

2019

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Background Per- and polyfluoroalkyl substances (PFASs) are environmentally persistent and bioaccumulative chemicals. Immunomodulation is among the most concerning of toxic effects linked with PFAS exposure in mammalian models. However, no studies had yet shown this to be true in birds. Thus, we designed and conducted the first study to determine if PFASs could cause immunomodulation in birds. Secondly, we wanted to determine the effects on an avian host when exposed not only to immunomodulating chemicals, but also to a viral challenge. The aim, to determine if PFAS mediated immunmodulation functionally affects a pathogen challenge for a host. As innate immune system signalling pathways initiate crucial responses against a pathogen challenge, and are lesser studied than their adaptive counterparts, we focused on these pathways. To provide the first information on this, an in vitro experiment was designed and performed using chicken embryo fibroblasts exposed to perfluorooctane sulfonate (PFOS) (22 ppm) and immune markers characterised before and after being infected with gallid herpesvirus-2 (GaHV-2). Results The expression of two pro-inflammatory cytokines, namely interleukin 8 (IL-8) and tumor necrosis factor alpha (TNF-α), the nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells (NF-κB), and the anti-inflammatory cytokine interleukin 4 (IL-4) were investigated in various scenarios. These results showed that exposure to PFOS decreased immune gene expression in chicken fibroblasts from 36 h post-exposure. Next, it was shown that this decrease could be mitigated by infection with gallid herpesvirus-2, which increased gene expression back to the baseline/control levels. Conclusions Not only is this the first study to provide the expected evidence that PFOS has immunomodulatory potential in birds, it also provides unexpected data that virus infections can mitigate this negative effect. Thereby, further research, including in vivo and in situ studies, on the impact of PFOS on host-virus interactions is now warranted, as it has been overlooked and might contribute to our understanding of recent disease outbreaks in wildlife. The mechanisms by which gallid herpesvirus mitigates immunomodulation were beyond the scope of this study, but are now of interest for future study. Electronic supplementary material The online version of this article (10.1186/s12917-019-1953-2) contains supplementary material, which is available to authorized users.

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“…However, additional signals provided by GaHV-2, like the production of DAMPs, might (in contrast to in poly(I:C)-treated cells) be a reason for the significant expression of TLR3-induced defense mechanisms like the activation of NF-jB signaling. One study revealed that TLR3-mediated anti-viral effects in GaHV-2-infected CEF were associated with production of inflammatory cytokines (Zou et al 2017). Therefore, modulation of NF-jB signaling pathways was expected to represent an important target during GaHV-2 infection.…”

Section: Responses To Infection With Gahv-2mentioning

confidence: 99%

Environmental pollutants modulate RNA and DNA virus-activated miRNA-155 expression and innate immune system responses: Insights into new immunomodulative mechanisms*

Badry

Jaspers

Waugh

2020

Journal of Immunotoxicology

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Many persistent organic pollutants, such as polychlorinated biphenyls (PCBs), have high immunomodulating potentials. Exposure to them, in combination with virus infections, has been shown to aggravate outcomes of the infection, leading to increased viral titers and host mortality. Expression of immune-related microRNA (miR) signaling pathways (by host and/or virus) have been shown to be important in determining these outcomes; there is some evidence to suggest pollutants can cause dysregulation of miRNAs. It was thus hypothesized here that modulation of miRNAs (and associated cytokine genes) by pollutants exerts negative effects during viral infections. To test this, an in vitro study on chicken embryo fibroblasts (CEF) exposed to a PCB mixture (Aroclor 1260) and then stimulated with a synthetic RNA virus (poly(I:C)) or infected with a lymphoma-causing DNA virus (Gallid Herpes Virus 2 [GaHV-2]) was conducted. Using quantitative real-time PCR, expression patterns for mir-155, pro-inflammatory TNFa and IL-8, transcription factor NF-jB1, and anti-inflammatory IL-4 were investigated 8, 12, and 18 h after virus activation. The study showed that Aroclor1260 modulated mir-155 expression, such that a down-regulation of mir-155 in poly(

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Toll-like receptor 3 pathway restricts Marek’s disease virus infection

Cited by 12 publications

References 31 publications

Single stranded (ss)RNA-mediated antiviral response against infectious laryngotracheitis virus infection

Single stranded (ss)RNA-mediated antiviral response against infectious laryngotracheitis virus infection

PFOS mediates immunomodulation in an avian cell line that can be mitigated via a virus infection

Environmental pollutants modulate RNA and DNA virus-activated miRNA-155 expression and innate immune system responses: Insights into new immunomodulative mechanisms*

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