scholarly journals IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection

2010 ◽  
Vol 185 (9) ◽  
pp. 5056-5065 ◽  
Author(s):  
Wei Li ◽  
Wei Sun ◽  
Li Liu ◽  
Fang Yang ◽  
Yongkui Li ◽  
...  
Keyword(s):  
Virus Infection ◽  
Viral Replication ◽  
Influenza A Virus ◽  
Influenza A ◽  
Epigenetic Modifications ◽  
Influenza A Virus Infection ◽  
Proinflammatory Factor

scholarly journals Itaconate and derivatives reduce interferon responses and inflammation in influenza A virus infection

2021 ◽  
Author(s):  
Aaqib Sohail ◽  
Azeem A. Iqbal ◽  
Nishika Sahini ◽  
Mohamed Tantawy ◽  
Moritz Winterhoff ◽  
...  
Keyword(s):  
Virus Infection ◽  
Viral Replication ◽  
Influenza A Virus ◽  
Influenza A ◽  
Pulmonary Inflammation ◽  
Transcriptome Profiling ◽  
Host Responses ◽  
Monocytes And Macrophages ◽  
Influenza A Virus Infection ◽  
Interferon Responses

AbstractItaconate has recently emerged as a metabolite with immunomodulatory properties. We evaluated effects of endogenous itaconate and exogenous itaconate, dimethyl-, and 4-octyl-itaconate on host responses to influenza A virus infection. Infection induced ACOD1 (the enzyme catalyzing itaconate synthesis) mRNA in monocytes and macrophages, which correlated with viral replication and was abrogated by itaconate treatment. Pulmonary inflammation and weight loss were greater in Acod1-/- than wild-type mice, and ectopic synthesis of itaconate in human epithelial cells reduced infection-induced inflammation. The compounds induced different recruitment programs in infected human macrophages, and transcriptome profiling revealed that they reversed infection-triggered interferon responses and modulated inflammation in cell lines, PBMC, and lung tissue. Single-cell RNA sequencing of PBMC revealed that infection induced ACOD1 exclusively in monocytes, whereas treatment silenced IFN-responses in monocytes, lymphocytes, and NK cells. Viral replication did not increase under treatment despite the dramatically repressed IFN responses, but 4-octyl itaconate inhibited viral transcription in PBMC. The results reveal dramatic reprogramming of host responses by itaconate and derivatives and their potential as adjunct treatments for hyperinflammation in viral infection.

scholarly journals Human Properdin Released By Infiltrating Neutrophils Can Modulate Influenza A Virus Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Praveen M. Varghese ◽  
Shuvechha Mukherjee ◽  
Futwan A. Al-Mohanna ◽  
Souad M. Saleh ◽  
Fahad N. Almajhdi ◽  
...  
Keyword(s):  
Virus Infection ◽  
Inflammatory Response ◽  
Viral Replication ◽  
Influenza A Virus ◽  
Influenza A ◽  
Alternative Pathway ◽  
A549 Cells ◽  
H1n1 Subtype ◽  
H3n2 Subtype ◽  
Influenza A Virus Infection

The complement system is designed to recognise and eliminate invading pathogens via activation of classical, alternative and lectin pathways. Human properdin stabilises the alternative pathway C3 convertase, resulting in an amplification loop that leads to the formation of C5 convertase, thereby acting as a positive regulator of the alternative pathway. It has been noted that human properdin on its own can operate as a pattern recognition receptor and exert immune functions outside its involvement in complement activation. Properdin can bind directly to microbial targets via DNA, sulfatides and glycosaminoglycans, apoptotic cells, nanoparticles, and well-known viral virulence factors. This study was aimed at investigating the complement-independent role of properdin against Influenza A virus infection. As one of the first immune cells to arrive at the site of IAV infection, we show here that IAV challenged neutrophils released properdin in a time-dependent manner. Properdin was found to directly interact with haemagglutinin, neuraminidase and matrix 1 protein Influenza A virus proteins in ELISA and western blot. Furthermore, modelling studies revealed that properdin could bind HA and NA of the H1N1 subtype with higher affinity compared to that of H3N2 due to the presence of an HA cleavage site in H1N1. In an infection assay using A549 cells, properdin suppressed viral replication in pH1N1 subtype while promoting replication of H3N2 subtype, as revealed by qPCR analysis of M1 transcripts. Properdin treatment triggered an anti-inflammatory response in H1N1-challenged A549 cells and a pro-inflammatory response in H3N2-infected cells, as evident from differential mRNA expression of TNF-α, NF-κB, IFN-α, IFN-β, IL-6, IL-12 and RANTES. Properdin treatment also reduced luciferase reporter activity in MDCK cells transduced with H1N1 pseudotyped lentiviral particles; however, it was increased in the case of pseudotyped H3N2 particles. Collectively, we conclude that infiltrating neutrophils at the site of IAV infection can release properdin, which then acts as an entry inhibitor for pandemic H1N1 subtype while suppressing viral replication and inducing an anti-inflammatory response. H3N2 subtype can escape this immune restriction due to altered haemagglutinin and neuraminindase, leading to enhanced viral entry, replication and pro-inflammatory response. Thus, depending on the subtype, properdin can either limit or aggravate IAV infection in the host.

scholarly journals Up-regulation of microRNA-203 in influenza A virus infection inhibits viral replication by targeting DR1

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sen Zhang ◽  
Jing Li ◽  
Junfeng Li ◽  
Yinhui Yang ◽  
Xiaoping Kang ◽  
...  
Keyword(s):  
Virus Infection ◽  
Viral Replication ◽  
Influenza A Virus ◽  
Influenza A ◽  
Influenza A Virus Infection

scholarly journals Induction of cyclophilin A by influenza A virus infection facilitates group A Streptococcus coinfection

Cell Reports ◽  
2021 ◽  
Vol 35 (7) ◽  
pp. 109159
Author(s):  
Xiaoyuan Bai ◽  
Wenxian Yang ◽  
Xiaohan Luan ◽  
Huizi Li ◽  
Heqiao Li ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Group A Streptococcus ◽  
Cyclophilin A ◽  
Group A ◽  
Influenza A Virus Infection

scholarly journals Dicer is involved in protection against influenza A virus infection

2007 ◽  
Vol 88 (10) ◽  
pp. 2627-2635 ◽  
Author(s):  
Alexey A. Matskevich ◽  
Karin Moelling
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Mammalian Cells ◽  
Influenza A ◽  
Virus Production ◽  
Vero Cells ◽  
Antiviral Response ◽  
Protein Levels ◽  
Infected Cells ◽  
Influenza A Virus Infection

In mammals the interferon (IFN) system is a central innate antiviral defence mechanism, while the involvement of RNA interference (RNAi) in antiviral response against RNA viruses is uncertain. Here, we tested whether RNAi is involved in the antiviral response in mammalian cells. To investigate the role of RNAi in influenza A virus-infected cells in the absence of IFN, we used Vero cells that lack IFN-α and IFN-β genes. Our results demonstrate that knockdown of a key RNAi component, Dicer, led to a modest increase of virus production and accelerated apoptosis of influenza A virus-infected cells. These effects were much weaker in the presence of IFN. The results also show that in both Vero cells and the IFN-producing alveolar epithelial A549 cell line influenza A virus targets Dicer at mRNA and protein levels. Thus, RNAi is involved in antiviral response, and Dicer is important for protection against influenza A virus infection.

scholarly journals A Functional Variation in CD55 Increases the Severity of 2009 Pandemic H1N1 Influenza A Virus Infection

2012 ◽  
Vol 206 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Jie Zhou ◽  
Kelvin Kai-Wang To ◽  
Hui Dong ◽  
Zhong-Shan Cheng ◽  
Candy Choi-Yi Lau ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
H1n1 Influenza ◽  
Pandemic H1n1 ◽  
Functional Variation ◽  
Pandemic H1n1 Influenza ◽  
Influenza A Virus Infection
Sign in / Sign up

Export Citation Format

Share Document