Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits

Berri, Fatma; Lê, Vuong Ba; Jandrot‐Perrus, Martine; Lina, Bruno; Riteau, Béatrice

doi:10.1007/s00018-013-1479-x

Cited by 36 publications

(33 citation statements)

References 123 publications

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“…Riteau and colleagues recently proposed that PAR1 may play a protective role in "non-severe IAV infection" where it cooperates with PRRs to eliminate the pathogen. 79 However, during "severe IAV infection," PAR1 may enhance inflammation. This model suggests that PAR1 can be protective or deleterious depending on the dose of IAV.…”

Section: Role Of Par2 In Iav Infection In Micementioning

confidence: 99%

Multiple roles of the coagulation protease cascade during virus infection

Antoniak

Mackman

2014

Blood

192

205

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The coagulation cascade is activated during viral infections. This response may be part of the host defense system to limit spread of the pathogen. However, excessive activation of the coagulation cascade can be deleterious. In fact, inhibition of the tissue factor/factor VIIa complex reduced mortality in a monkey model of Ebola hemorrhagic fever. Other studies showed that incorporation of tissue factor into the envelope of herpes simplex virus increases infection of endothelial cells and mice. Furthermore, binding of factor X to adenovirus serotype 5 enhances infection of hepatocytes but also increases the activation of the innate immune response to the virus. Coagulation proteases activate protease-activated receptors (PARs). Interestingly, we and others found that PAR1 and PAR2 modulate the immune response to viral infection. For instance, PAR1 positively regulates TLR3-dependent expression of the antiviral protein interferon β, whereas PAR2 negatively regulates expression during coxsackievirus group B infection. These studies indicate that the coagulation cascade plays multiple roles during viral infections.

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Section: Role Of Par2 In Iav Infection In Micementioning

confidence: 99%

Multiple roles of the coagulation protease cascade during virus infection

Antoniak

Mackman

2014

Blood

192

205

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“…The M2 protein has been shown to induce secretion of the pyrogenic cytokine IL-1β via stimulation of the NLRP3 inflammasome pathway [16]. This may contribute to uncontrolled deleterious inflammation (so-called cytokine storm) which may exacerbate lung immunopathology and disease of influenza [3]. Furthermore, IL-1 plays an important role in hemostasis deregulation through tissue factor induction.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, IL-1 plays an important role in hemostasis deregulation through tissue factor induction. Since hemostasis deregulation emerges as a key pathway in cytokine storm induced by influenza viruses [3,4,18], it seems reasonable to speculate that human signature residues in the M2 protein of AIVs may be involved in cytokine storm via IL-1 production and hemostasis deregulation.…”

Section: Discussionmentioning

confidence: 99%

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The zoonotic potential of avian influenza viruses isolated from wild waterfowl in Zambia

et al. 2014

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Whilst remarkable progress in elucidating the mechanisms governing interspecies transmission and pathogenicity of highly pathogenic avian influenza viruses (AIVs) have been made, similar studies focusing on low pathogenic AIVs isolated from the wild waterfowl reservoir are limited.We previously reported that two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues. To further substantiate these observations, we infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all the tested strains replicated poorly and were nonpathogenic for chickens. In contrast, most of the strains having human signatures replicated well in the lungs of mice, and one of these strains caused severe illness in mice and induced lung injury that was characterized by a severe accumulation of polymorphonuclear leukocytes. These results suggest that some strains tested in this study may have the potential to directly infect mammalian hosts without adaptation, which might possibly be associated with the possession of human signature residues. Close monitoring and evaluation of host-associated signatures may help elucidate the prevalence and emergence of AIVs with potential of causing zoonotic infections.

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“…Thus, these viruses are of great concern to human health and impose a considerable socioeconomic burden. Important factors in the pathogenesis of influenza include the efficient replication of the virus in the respiratory tract and the host immune response, traits that are dependent on each other (4)(5)(6). While the immune response aims to control the spread of the virus, IAV has developed strategies for subverting host defenses, thereby facilitating their spread (7)(8)(9)(10).…”

mentioning

confidence: 99%

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

Berri

Haffar

Lê

et al. 2014

J Virol

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During the budding process, influenza A viruses (IAVs) incorporate multiple host cell membrane proteins. However, for most of them, their significance in viral morphogenesis and infectivity remains unknown. We demonstrate here that the expression of annexin V (A5) is upregulated at the cell surface upon IAV infection and that a substantial proportion of the protein is present in lipid rafts, the site of virus budding. Western blotting and immunogold analysis of highly purified IAV particles showed the presence of A5 in the virion. Significantly, gamma interferon (IFN-␥)-induced Stat phosphorylation and IFN-␥-induced 10-kDa protein (IP-10) production in macrophage-derived THP-1 cells was inhibited by purified IAV particles. Disruption of the IFN-␥ signaling pathway was A5 dependent since downregulation of its expression or its blockage reversed the inhibition and resulted in decreased viral replication in vitro. The functional significance of these results was also observed in vivo. Thus, IAVs can subvert the IFN-␥ antiviral immune response by incorporating A5 into their envelope during the budding process. IMPORTANCEMany enveloped viruses, including influenza A viruses, bud from the plasma membrane of their host cells and incorporate cellular surface proteins into viral particles. However, for the vast majority of these proteins, only the observation of their incorporation has been reported. We demonstrate here that the host protein annexin V is specifically incorporated into influenza virus particles during the budding process. Importantly, we showed that packaged annexin V counteracted the antiviral activity of gamma interferon in vitro and in vivo. Thus, these results showed that annexin V incorporated in the viral envelope of influenza viruses allow viral escape from immune surveillance. Understanding the role of host incorporated protein into virions may reveal how enveloped RNA viruses hijack the host cell machinery for their own purposes.

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Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits

Cited by 36 publications

References 123 publications

Multiple roles of the coagulation protease cascade during virus infection

Multiple roles of the coagulation protease cascade during virus infection

The zoonotic potential of avian influenza viruses isolated from wild waterfowl in Zambia

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

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