ArticlePLoS pathogens2014
Deficient IFN signaling by myeloid cells leads to MAVS-dependent virus-induced sepsis.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 72 citations in OpenAlex.
- Type I and III interferon responses restrict infection by tick-borne orthoflaviviruses through IFI6.Journal of virology · 2026Article
- MyD88 signaling in myeloid cells induces gastrointestinal tract injury and systemic inflammation after West Nile virus infection.Cell reports · 2026Article
- Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.Pflugers Archiv : European journal of physiology · 2026Article
- Equine lentivirus Gag protein degrades mitochondrial antiviral signaling protein via the E3 ubiquitin ligase Smurf1.Journal of virology · 2025Article
- MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis.Frontiers in cellular and infection microbiology · 2025Article
- Viral sepsis: diagnosis, clinical features, pathogenesis, and clinical considerations.Military Medical Research · 2024Review
- Type I interferon signaling in dendritic cells limits direct antigen presentation and CD8mBio · 2024Article
- Single-cell analysis reveals an antiviral network that controls Zika virus infection in human dendritic cells.Journal of virology · 2024Article
- Blockade of interferon signaling decreases gut barrier integrity and promotes severe West Nile virus disease.Nature communications · 2023Article
- Clodronate is not protective in lethal viral encephalitis despite substantially reducing inflammatory monocyte infiltration in the CNS.Frontiers in immunology · 2023Article
- Mitochondrial antiviral signaling protein: a potential therapeutic target in renal disease.Frontiers in immunology · 2023Review
- Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.Frontiers in immunology · 2023Article
- Emerging roles of the complement system in host-pathogen interactions.Trends in microbiology · 2022Review
- STING1 in sepsis: Mechanisms, functions, and implications.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2022Review
- Endogenous Retroviruses (ERVs): Does RLR (RIG-I-Like Receptors)-MAVS Pathway Directly Control Senescence and Aging as a Consequence of ERV De-Repression?Frontiers in immunology · 2022Review
- Shiftless inhibits flavivirus replication in vitro and is neuroprotective in a mouse model of Zika virus pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Pathogenicity and virulence of West Nile virus revisited eight decades after its first isolation.Virulence · 2021Article
- The MAVS Immune Recognition Pathway in Viral Infection and Sepsis.Antioxidants & redox signaling · 2021Review
- Type I IFN signaling limits hemorrhage-like disease after infection with Japanese encephalitis virus through modulating a prerequisite infection of CD11bJournal of neuroinflammation · 2021Article
- mRNA induced expression of human angiotensin-converting enzyme 2 in mice for the study of the adaptive immune response to severe acute respiratory syndrome coronavirus 2.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The type I interferon (IFN) signaling response limits infection of many RNA and DNA viruses. To define key cell types that require type I IFN signaling to orchestrate immunity against West Nile virus (WNV), we infected mice with conditional deletions of the type I IFN receptor (IFNAR) gene. Deletion of the Ifnar gene in subsets of myeloid cells resulted in uncontrolled WNV replication, vasoactive cytokine production, sepsis, organ damage, and death that were remarkably similar to infection of Ifnar-/- mice completely lacking type I IFN signaling. In Mavs-/-×Ifnar-/- myeloid cells and mice lacking both Ifnar and the RIG-I-like receptor adaptor gene Mavs, cytokine production was muted despite high levels of WNV infection. Thus, in myeloid cells, viral infection triggers signaling through MAVS to induce proinflammatory cytokines that can result in sepsis and organ damage. Viral pathogenesis was caused in part by massive complement activation, as liver damage was minimized in animals lacking complement components C3 or factor B or treated with neutralizing anti-C5 antibodies. Disease in Ifnar-/- and CD11c Cre+Ifnarf/f mice also was facilitated by the proinflammatory cytokine TNF-α, as blocking antibodies diminished complement activation and prolonged survival without altering viral burden. Collectively, our findings establish the dominant role of type I IFN signaling in myeloid cells in restricting virus infection and controlling pathological inflammation and tissue injury.
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