Antiviral Response Induced by Toll-Like Receptor (TLR) 7/TLR8 Activation Inhibits Human Immunodeficiency Virus Type 1 Infection in Cord Blood Macrophages

Pietrobon, Anna Julia; Yoshikawa, Fabio Seiti Yamada; Oliveira, Luana M; Pereira, Newton Lindolfo; Matozo, Tais; Alencar, Bruna Cunha de; Duarte, Alberto J. S.; Sato, Maria Notomi

doi:10.1093/infdis/jiab389

Cited by 8 publications

(2 citation statements)

References 39 publications

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“…Activation of TLR8 recruits the homologous domain containing adaptor MyD88, which attracts and activates the protein kinases IRAK4 and IRAK2. These kinases activate the downstream binding molecule TRAF6, which activates the IKKα/β/γ complex leading to the activation of NF-κB and expression of inflammatory genes driven by NF-κB [9]. TLR8 is located in the endosome and the TLR8-NF-κB signaling pathway has antibacterial and antiviral effects [10].…”

Section: Introductionmentioning

confidence: 99%

African Swine Fever Virus A528R Inhibits TLR8 Mediated NF-κB Activity by Targeting p65 Activation and Nuclear Translocation

Liu

Jiang

et al. 2021

Viruses

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African swine fever (ASF) is mainly an acute hemorrhagic disease which is highly contagious and lethal to domestic pigs and wild boars. The global pig industry has suffered significant economic losses due to the lack of an effective vaccine and treatment. The African swine fever virus (ASFV) has a large genome of 170–190 kb, encoding more than 150 proteins. During infection, ASFV evades host innate immunity via multiple viral proteins. A528R is a very important member of the polygene family of ASFV, which was shown to inhibit IFN-β production by targeting NF-κB, but its mechanism is not clear. This study has shown that A528R can suppress the TLR8-NF-κB signaling pathway, including the inhibition of downstream promoter activity, NF-κB p65 phosphorylation and nuclear translocation, and the antiviral and antibacterial activity. Further, we found the cellular co-localization and interaction between A528R and p65, and ANK repeat domains of A528R and RHD of p65 are involved in their interaction and the inhibition of p65 activity. Therefore, we conclude that A528R inhibits TLR8-NF-κB signaling by targeting p65 activation and nuclear translocation.

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Section: Introductionmentioning

confidence: 99%

African Swine Fever Virus A528R Inhibits TLR8 Mediated NF-κB Activity by Targeting p65 Activation and Nuclear Translocation

Liu

Jiang

et al. 2021

Viruses

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“…O nosso grupo de pesquisa vem estudando a sinalização via TLR7/TLR8 (dímero CL097) em vários modelos, para restaurar a resposta de IFN tipo I em infecções virais como HIV-1 (Cardoso, Pereira et al 2013, Lima, Oliveira et al 2017, Pietrobon, Yoshikawa et al 2022, doenças cutâneas como o líquen plano (Domingues, de Carvalho et al 2016, Domingues, Pietrobon et al 2019) e síndrome de Sezary (Manfrere, Torrealba et al 2016). O estudo envolvendo envelhecimento, no entanto, ainda não foi explorado pelo nosso grupo.…”

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Inflammaging: investigação sobre envelhecimento cutâneo, imunossenescência e SARS-CoV-2

Fernandes

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Agradeço em primeiro lugar a Deus, a todos os eventos do Universo e à força que me conduziu até aqui. Apesar de cientista, tenho certeza que, acima de tudo, existe algo muito maior e divino que nos ilumina e nos conduz para a evolução em todos os sentidos, se assim permitirmos. Agradeço à Profa. Dra. Maria Notomi Sato, orientadora desse e de tantos outros trabalhos brilhantes, que, desde o momento em que pisei no LIM-56, já se mostrou uma pessoa extremamente receptiva, acolhedora e uma excelente pesquisadora.Minha admiração foi imediata e só cresceu ao longo desses anos de orientação e parceria. Obrigada por sempre estar presente em todas as etapas da nossa formação enquanto alunos de pós-graduação e seres humanos, pelas colocações, correções de manuscritos (não foram poucas!) e compreensão.

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The battle between host antiviral innate immunity and immune evasion by cytomegalovirus

Li,

Xie,

et al. 2024

Cell. Mol. Life Sci.

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Cytomegalovirus (CMV) has successfully established a long-lasting latent infection in humans due to its ability to counteract the host antiviral innate immune response. During coevolution with the host, the virus has evolved various evasion techniques to evade the host’s innate immune surveillance. At present, there is still no vaccine available for the prevention and treatment of CMV infection, and the interaction between CMV infection and host antiviral innate immunity is still not well understood. However, ongoing studies will offer new insights into how to treat and prevent CMV infection and its related diseases. Here, we update recent studies on how CMV evades antiviral innate immunity, with a focus on how CMV proteins target and disrupt critical adaptors of antiviral innate immune signaling pathways. This review also discusses some classic intrinsic cellular defences that are crucial to the fight against viral invasion. A comprehensive review of the evasion mechanisms of antiviral innate immunity by CMV will help investigators identify new therapeutic targets and develop vaccines against CMV infection.

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Antiviral Response Induced by Toll-Like Receptor (TLR) 7/TLR8 Activation Inhibits Human Immunodeficiency Virus Type 1 Infection in Cord Blood Macrophages

Cited by 8 publications

References 39 publications

African Swine Fever Virus A528R Inhibits TLR8 Mediated NF-κB Activity by Targeting p65 Activation and Nuclear Translocation

African Swine Fever Virus A528R Inhibits TLR8 Mediated NF-κB Activity by Targeting p65 Activation and Nuclear Translocation

Inflammaging: investigação sobre envelhecimento cutâneo, imunossenescência e SARS-CoV-2

The battle between host antiviral innate immunity and immune evasion by cytomegalovirus

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