scholarly journals Baicalin inhibits TLR7/MYD88 signaling pathway activation to suppress lung inflammation in mice infected with influenza A virus

2014 ◽  
Vol 2 (3) ◽  
pp. 437-441 ◽  
Author(s):  
QIAOFENG WAN ◽  
HAO WANG ◽  
XUEBO HAN ◽  
YUAN LIN ◽  
YANHUI YANG ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Lung Inflammation ◽  
Influenza A ◽  
Pathway Activation ◽  
Myd88 Signaling

scholarly journals Host Non-Coding RNA Regulates Influenza A Virus Replication

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 51
Author(s):  
Yuejiao Liao ◽  
Shouqing Guo ◽  
Geng Liu ◽  
Zhenyu Qiu ◽  
Jiamin Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Influenza A ◽  
Janus Kinase ◽  
Research Progress ◽  
Receptor Signaling ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Non Coding Rnas ◽  
Virus Interactions

Outbreaks of influenza, caused by the influenza A virus (IAV), occur almost every year in various regions worldwide, seriously endangering human health. Studies have shown that host non-coding RNA is an important regulator of host–virus interactions in the process of IAV infection. In this paper, we comprehensively analyzed the research progress on host non-coding RNAs with regard to the regulation of IAV replication. According to the regulation mode of host non-coding RNAs, the signal pathways involved, and the specific target genes, we found that a large number of host non-coding RNAs directly targeted the PB1 and PB2 proteins of IAV. Nonstructural protein 1 and other key genes regulate the replication of IAV and indirectly participate in the regulation of the retinoic acid-induced gene I-like receptor signaling pathway, toll-like receptor signaling pathway, Janus kinase signal transducer and activator of transcription signaling pathway, and other major intracellular viral response signaling pathways to regulate the replication of IAV. Based on the above findings, we mapped the regulatory network of host non-coding RNAs in the innate immune response to the influenza virus. These findings will provide a more comprehensive understanding of the function and mechanism of host non-coding RNAs in the cellular anti-virus response as well as clues to the mechanism of cell–virus interactions and the discovery of antiviral drug targets.

scholarly journals Novel endosomal NOX2 oxidase inhibitor ameliorates pandemic influenza A virus‐induced lung inflammation in mice

Respirology ◽  
2019 ◽  
Vol 24 (10) ◽  
pp. 1011-1017 ◽  
Author(s):  
Eunice E. To ◽  
Raymond Luong ◽  
Jiayin Diao ◽  
John J. O’ Leary ◽  
Doug A. Brooks ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Pandemic Influenza ◽  
Lung Inflammation ◽  
Influenza A ◽  
Oxidase Inhibitor

scholarly journals Hemagglutinin of Influenza A Virus Antagonizes Type I Interferon (IFN) Responses by Inducing Degradation of Type I IFN Receptor 1

2015 ◽  
Vol 90 (5) ◽  
pp. 2403-2417 ◽  
Author(s):  
Chuan Xia ◽  
Madhuvanthi Vijayan ◽  
Curtis J. Pritzl ◽  
Serge Y. Fuchs ◽  
Adrian B. McDermott ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Influenza A ◽  
Type I Interferon ◽  
Innate Immune ◽  
Host Cells ◽  
Type I ◽  
Type I Ifn ◽  
Type I Ifns ◽  
Ha Protein

ABSTRACTInfluenza A virus (IAV) employs diverse strategies to circumvent type I interferon (IFN) responses, particularly by inhibiting the synthesis of type I IFNs. However, it is poorly understood if and how IAV regulates the type I IFN receptor (IFNAR)-mediated signaling mode. In this study, we demonstrate that IAV induces the degradation of IFNAR subunit 1 (IFNAR1) to attenuate the type I IFN-induced antiviral signaling pathway. Following infection, the level of IFNAR1 protein, but not mRNA, decreased. Indeed, IFNAR1 was phosphorylated and ubiquitinated by IAV infection, which resulted in IFNAR1 elimination. The transiently overexpressed IFNAR1 displayed antiviral activity by inhibiting virus replication. Importantly, the hemagglutinin (HA) protein of IAV was proved to trigger the ubiquitination of IFNAR1, diminishing the levels of IFNAR1. Further, influenza A viral HA1 subunit, but not HA2 subunit, downregulated IFNAR1. However, viral HA-mediated degradation of IFNAR1 was not caused by the endoplasmic reticulum (ER) stress response. IAV HA robustly reduced cellular sensitivity to type I IFNs, suppressing the activation of STAT1/STAT2 and induction of IFN-stimulated antiviral proteins. Taken together, our findings suggest that IAV HA causes IFNAR1 degradation, which in turn helps the virus escape the powerful innate immune system. Thus, the research elucidated an influenza viral mechanism for eluding the IFNAR signaling pathway, which could provide new insights into the interplay between influenza virus and host innate immunity.IMPORTANCEInfluenza A virus (IAV) infection causes significant morbidity and mortality worldwide and remains a major health concern. When triggered by influenza viral infection, host cells produce type I interferon (IFN) to block viral replication. Although IAV was shown to have diverse strategies to evade this powerful, IFN-mediated antiviral response, it is not well-defined if IAV manipulates the IFN receptor-mediated signaling pathway. Here, we uncovered that influenza viral hemagglutinin (HA) protein causes the degradation of type I IFN receptor subunit 1 (IFNAR1). HA promoted phosphorylation and polyubiquitination of IFNAR1, which facilitated the degradation of this receptor. The HA-mediated elimination of IFNAR1 notably decreased the cells' sensitivities to type I IFNs, as demonstrated by the diminished expression of IFN-induced antiviral genes. This discovery could help us understand how IAV regulates the host innate immune response to create an environment optimized for viral survival in host cells.

TLR4-MyD88 signaling pathway is responsible for acute lung inflammation induced by reclaimed water

2020 ◽  
Vol 396 ◽  
pp. 122586 ◽  
Author(s):  
Gang Liu ◽  
Yun Lu ◽  
Liangliang Shi ◽  
Yunru Ren ◽  
Jiayang Kong ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Lung Inflammation ◽  
Reclaimed Water ◽  
Acute Lung Inflammation ◽  
Myd88 Signaling

Microbiota Regulates the TLR7 Signaling Pathway Against Respiratory Tract Influenza A Virus Infection

2013 ◽  
Vol 67 (4) ◽  
pp. 414-422 ◽  
Author(s):  
Sha Wu ◽  
Zhen-You Jiang ◽  
Yi-Fan Sun ◽  
Bin Yu ◽  
Jia Chen ◽  
...  
Keyword(s):  
Virus Infection ◽  
Respiratory Tract ◽  
Signaling Pathway ◽  
Influenza A Virus ◽  
Influenza A ◽  
Influenza A Virus Infection
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