Recent advances on viral manipulation of NF-κB signaling pathway

Zhao, Jun; He, Shuchang; Minassian, Arlet; Li, Junhua; Feng, Pinghui

doi:10.1016/j.coviro.2015.08.013

Cited by 73 publications

(57 citation statements)

References 84 publications

(87 reference statements)

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“…This feedback positively elevates the cell susceptibility to EBV entry . The similar effects mediated by the KSHV vFLIP protein and HTLV‐1 Tax protein, indirectly or directly, activate IKK complex and, consequently, NF‐κB to enhance the oncogenic transformation . Venuti and colleagues found that overexpression of miR‐146a during HSV‐1 replication is strictly dependent on the activation of NF‐κB and related to tight control of IRAK1.…”

Section: Mir‐146a In Herpesvirusesmentioning

confidence: 99%

“…For example, the polymerase of HBV and hepatitis A virus (HAV) 3C protein prevent the activity of the trimeric IκB kinase (IKK) complex, which is the core component of NF‐κB activation. HSV‐1, EBV, vaccinia virus, and poxvirus inhibit, indirectly or directly, nuclear translocation of NF‐κB p65 representing a critical step to maintain the antiviral response mediated by NF‐κB . Therefore, during the virus‐host coevolution, the virus has developed many strategies to inhibit NF‐κB activity and promote survival of the virus‐infected cell.…”

Section: Mir‐146a In Herpesvirusesmentioning

confidence: 99%

“…HSV-1, EBV, vaccinia virus, and poxvirus inhibit, indirectly or directly, nuclear translocation of NF-κB p65 representing a critical step to maintain the antiviral response mediated by NF-κB. 129 Therefore, during the virus-host coevolution, the virus has developed many strategies to inhibit NF-κB activity and promote survival of the virus-infected cell. Contrariwise, some virus families lead to persistently enhance the NF-κB activation tightly connected with oncogenic transformation.…”

Section: Mir-146a In Herpesvirusesmentioning

confidence: 99%

“…130 The similar effects mediated by the KSHV vFLIP protein and HTLV-1 Tax protein, indirectly or directly, activate IKK complex and, consequently, NF-κB to enhance the oncogenic transformation. 129 Venuti and colleagues 62 found that overexpression of miR-146a during HSV-1 replication is strictly dependent on the activation of NF-κB and related to tight control of IRAK1. By using HSV-1 expressing the enhanced green fluorescent protein (EGFP) which is known as HSV-1\EGFP, they explored the ability of HSV-1 to recruit NF-κB, and HSV-1\EGFP elevates miR-146a expression in an NF-κBdependent manner in THP-1 cells.…”

Section: Mir-146a In Herpesvirusesmentioning

confidence: 99%

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The role of miR‐146a in viral infection

et al. 2019

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Cellular microRNAs (miRNAs) were identified as a key player in the posttranscriptional regulation of cellular‐genes regulatory pathways. They also emerged as a significant regulator of the immune response. In particular, miR‐146a acts as an importance modulator of function and differentiation cells of the innate and adaptive immunity. It has been associated with disorder including cancer and viral infections. Given its significance in the regulation of key cellular processes, it is not surprising which virus infection have found ways to dysregulation of miRNAs. miR‐146a has been identified in exosomes (exosomal miR‐146a). After the exosomes release from donor cells, they are taken up by the recipient cell and probably the exosomal miR‐146a is able to modulate the antiviral response in the recipient cell and result in making them more susceptible to virus infection. In this review, we discuss recent reports regarding miR‐146a expression levels, target genes, function, and contributing role in the pathogenesis of the viral infection and provide a clue to develop the new therapeutic and preventive strategies for viral disease in the future.

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Section: Mir‐146a In Herpesvirusesmentioning

confidence: 99%

Section: Mir‐146a In Herpesvirusesmentioning

confidence: 99%

Section: Mir-146a In Herpesvirusesmentioning

confidence: 99%

Section: Mir-146a In Herpesvirusesmentioning

confidence: 99%

See 2 more Smart Citations

The role of miR‐146a in viral infection

et al. 2019

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“…MuHV-4 evades IFN-I by targeting interferon regulatory factor 3 (IRF3) (23), TBK-1 (24), the IFN-I receptor (IFNAR) (25), STAT-1/2 (26), as well as other pathways (27) and associated defenses such as apoptosis/autophagy (28), NF-B (29), and PML (30,31). Nonetheless, disease in IFNAR-deficient mice (32,33) indicates IFN-I-dependent restraint.…”

Section: Human Gammaherpesviruses Cause Cancers By Infecting B Cellsmentioning

confidence: 99%

Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection

Lawler

Tan

Simas

et al. 2016

J Virol

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Gammaherpesviruses establish persistent, systemic infections and cause cancers. Murid herpesvirus 4 (MuHV-4) provides a unique window into the early events of host colonization. It spreads via lymph nodes. While dendritic cells (DC) pass MuHV-4 to lymph node B cells, subcapsular sinus macrophages (SSM), which capture virions from the afferent lymph, restrict its spread. Understanding how this restriction works offers potential clues to a more comprehensive defense. Type I interferon (IFN-I) blocked SSM lytic infection and reduced lytic cycle-independent viral reporter gene expression. Plasmacytoid DC were not required, but neither were SSM the only source of IFN-I, as IFN-I blockade increased infection in both intact and SSM-depleted mice. NK cells restricted lytic SSM infection independently of IFN-I, and SSM-derived virions spread to the spleen only when both IFN-I responses and NK cells were lacking. Thus, multiple innate defenses allowed SSM to adsorb virions from the afferent lymph with relative impunity. Enhancing IFN-I and NK cell recruitment could potentially also restrict DC infection and thus improve infection control. IMPORTANCE Human gammaherpesviruses cause cancers by infecting B cells. However, vaccines designed to block virus binding to B cells have not stopped infection. Using a related gammaherpesvirus of mice, we have shown that B cells are infected not via cell-free virus but via infected myeloid cells. This suggests a different strategy to stop B cell infection: stop virus production by myeloid cells. Not all myeloid infection is productive. We show that subcapsular sinus macrophages, which do not pass infection to B cells, restrict gammaherpesvirus production by recruiting type I interferons and natural killer cells. Therefore, a vaccine that speeds the recruitment of these defenses might stop B cell infection.E pstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) persist in B cells and cause cancers (1). Reducing their B cell infections is therefore an important therapeutic goal. Limited viral gene expression (2) makes established infections difficult to clear. The early events of host colonization may provide better targets. However, control mechanisms must be defined in vivo: inferring mechanisms from in vitro studies has proven problematic because immune function and its evasion are context dependent. Thus, EBV gp350-specific antibodies block B cell infection, and CD8 ϩ T cells kill infected B cells in vitro, but vaccinations to induce these effectors have not reduced infection rates (3).The early events of human infections are difficult to analyze because they predate clinical presentation (4). However, gammaherpesviruses long predate human speciation (5), and peak viral diversity in genes that interact with host-diverse functions suggests that viral coevolution has since acted to counter host divergence. Therefore, human and other mammalian gammaherpesviruses should colonize their hosts in similar ways. Murid herpesvirus 4 (MuHV-4) realistically infects la...

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Manipulation of Non-canonical NF-κB Signaling by Non-oncogenic Viruses

Struzik

Szulc-Dąbrowska

2018

Arch. Immunol. Ther. Exp.

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Nuclear factor (NF)-κB is a major regulator of antiviral response. Viral pathogens exploit NF-κB activation pathways to avoid cellular mechanisms that eliminate the infection. Canonical (classical) NF-κB signaling, which regulates innate immune response, cell survival and inflammation, is often manipulated by viral pathogens that can counteract antiviral response. Oncogenic viruses can modulate not only canonical, but also non-canonical (alternative) NF-κB activation pathways. The non-canonical NF-κB signaling is responsible for adaptive immunity and plays a role in lymphoid organogenesis, B cell development, as well as bone metabolism. Thus, non-canonical NF-κB activation has been linked to lymphoid malignancies. However, some data strongly suggest that the non-canonical NF-κB activation pathway may also function in innate immunity and is modulated by certain non-oncogenic viruses. Collectively, these findings show the importance of studying the impact of different groups of viral pathogens on alternative NF-κB activation. This mini-review focuses on the influence of non-oncogenic viruses on the components of non-canonical NF-κB signaling.

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Recent advances on viral manipulation of NF-κB signaling pathway

Cited by 73 publications

References 84 publications

The role of miR‐146a in viral infection

The role of miR‐146a in viral infection

Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection

Manipulation of Non-canonical NF-κB Signaling by Non-oncogenic Viruses

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