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Phosphatidylglycerol suppresses influenza A virus infection.

ABSTRACT: Influenza A virus (IAV) is a worldwide public health problem causing 500,000 deaths each year. Palmitoyl-oleoyl-phosphatidylglycerol (POPG) is a minor component of pulmonary surfactant, which has recently been reported to exert potent regulatory functions upon the innate immune system. In this article, we demonstrate that POPG acts as a strong antiviral agent against IAV. POPG markedly attenuated IL-8 production and cell death induced by IAV in cultured human bronchial epithelial cells. The lipid also suppressed viral attachment to the plasma membrane and subsequent replication in Madin-Darby canine kidney cells. Two virus strains, H1N1-PR8-IAV and H3N2-IAV, bind to POPG with high affinity, but exhibit only low-affinity interactions with the structurally related lipid, palmitoyl-oleoyl-phosphatidylcholine. Intranasal inoculation of H1N1-PR8-IAV in mice, in the presence of POPG, markedly suppressed the development of inflammatory cell infiltrates, the induction of IFN-γ recovered in bronchoalveolar lavage, and viral titers recovered from the lungs after 5 days of infection. These findings identify supplementary POPG as a potentially important new approach for treatment of IAV infections.

SUBMITTER: Numata M

PROVIDER: S-EPMC3359948 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Pulmonary surfactant phosphatidylglycerol inhibits respiratory syncytial virus-induced inflammation and infection.

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| S-EPMC2806703 | biostudies-literature

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| S-EPMC3778511 | biostudies-other

Influenza B Virus Infection Is Enhanced Upon Heterotypic Co-infection With Influenza A Virus.

Project description:Homotypic co-infections with influenza viruses are described to increase genetic population diversity, to drive viral evolution and to allow genetic complementation. Less is known about heterotypic co-infections between influenza A (IAV) and influenza B (IBV) viruses. Previous publications showed that IAV replication was suppressed upon co-infection with IBV. However, the effect of heterotypic co-infections on IBV replication was not investigated. To do so, we produced by reverse genetics a pair of replication-competent recombinant IAV (A/WSN/33) and IBV (B/Brisbane/60/2008) expressing a GFP and mCherry fluorescent reporter, respectively. A549 cells were infected simultaneously or 1 h apart at a high MOI with IAV-GFP or IBV-mCherry and the fluorescence was measured at 6 h post-infection by flow cytometry. Unexpectedly, we observed that IBV-mCherry infection was enhanced upon co-infection with IAV-GFP, and more strongly so when IAV was added 1 h prior to IBV. The same effect was observed with wild-type viruses and with various strains of IAV. Using UV-inactivated IAV or type-specific antiviral compounds, we showed that the enhancing effect of IAV infection on IBV infection was dependent on transcription/replication of the IAV genome. Our results, taken with available data in the literature, support the hypothesis that the presence of IAV proteins can enhance IBV genome expression and/or complement IBV defective particles.

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The host response to influenza virus infection

Project description:In this study, we performed a cross-species gene expression study of the peripheral blood from the Collaborative Cross (CC) mouse population after Influenza virus (IV).

2018-07-12 | GSE110384 | GEO

Toosendanin From Melia Fructus Suppresses Influenza A Virus Infection by Altering Nuclear Localization of Viral Polymerase PA Protein.

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| S-EPMC6757512 | biostudies-literature

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Project description:Volatile organic compounds (VOCs) emanating from humans have the potential to revolutionize non-invasive diagnostics. Yet, little is known about how these compounds are generated by complex biological systems, and even less is known about how these compounds are reflective of a particular physiological state. In this proof-of-concept study, we examined VOCs produced directly at the cellular level from B lymphoblastoid cells upon infection with three live influenza virus subtypes: H9N2 (avian), H6N2 (avian), and H1N1 (human). Using a single cell line helped to alleviate some of the complexity and variability when studying VOC production by an entire organism, and it allowed us to discern marked differences in VOC production upon infection of the cells. The patterns of VOCs produced in response to infection were unique for each virus subtype, while several other non-specific VOCs were produced after infections with all three strains. Also, there was a specific time course of VOC release post infection. Among emitted VOCs, production of esters and other oxygenated compounds was particularly notable, and these may be attributed to increased oxidative stress resulting from infection. Elucidating VOC signatures that result from the host cells response to infection may yield an avenue for non-invasive diagnostics and therapy of influenza and other viral infections.

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Influenza virus infection in racing greyhounds.

Project description: Not available

| S-EPMC3367648 | biostudies-literature

The dynamic proteome of Influenza A virus infection

Project description:We combined metabolic pulse labeling and quantitative shotgun proteomics to globally monitor protein synthesis upon infection of human cells with a human- and a bird-adapted IAV strain. While production of host proteins was remarkably similar, we observed striking differences in the kinetics of viral protein synthesis over the course of infection. Most importantly, the matrix protein M1 was inefficiently produced by the bird-adapted strain at later stages.

2019-11-11 | PXD011321 | Pride

Influenza virus infection causes global RNAPII termination defects

Project description:Viral infection perturbs host cells and can be used to uncover host regulatory mechanisms controlling both cell response and homeostasis. Here, using cell biological, biochemical and genetic tools, we reveal that influenza virus infection induces global transcriptional defects at the 3’-end of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. This effect induces the biogenesis of aberrant RNAs (3’-extensions and host gene fusions) which ultimately causes global transcriptional downregulation of physiological transcripts, an effect that impacts antiviral response and virulence. We show that this phenomenon occurs with multiple strains of influenza virus and it is dependent on influenza NS1 protein expression. Mechanistically, pervasive RNAPII run-through can be modulated by SUMOylation of an intrinsically disordered region (IDR) of the NS1 expressed by the 1918 pandemic influenza virus. SUMOylation increases NS1 partitioning in nuclear granules and interference with the host transcriptional apparatus which result in augmentation of termination defects and a concomitant increase in global host gene shut off. Our data identify a general strategy used by influenza virus to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins, along with human genetic variation in enzymes that metabolize post-translational modifications, can determine the outcome of an infection. We thus propose that analysis of strain-specific determinant of pathogenesis can shed light on the molecular basis of virulence.

2018-09-05 | GSE103604 | GEO

Screening of influenza A virus infection related microRNA

Project description:In the study presented here, A549 cells infected with influenza virus A /JingFang/86-1(H1N1) for 4 and 24 hours and intervention by Flutide, was used to acquire expression profiles of a total of 471 standard mature miRNAs based on Sanger miRBase Release 9.2.

2011-07-07 | GSE30421 | GEO

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