Abstract
The replication of viruses in secondary lymphoid organs guarantees sufficient amounts of pattern-recognition receptor ligands and antigens to activate the innate and adaptive immune system. Viruses with broad cell tropism usually replicate in lymphoid organs; however, whether a virus with a narrow tropism relies on replication in the secondary lymphoid organs to activate the immune system remains not well studied. In this study, we used the artificial intravenous route of infection to determine whether Influenza A virus (IAV) replication can occur in secondary lymphatic organs (SLO) and whether such replication correlates with innate immune activation. Indeed, we found that IAV replicates in secondary lymphatic tissue. IAV replication was dependent on the expression of Sialic acid residues in antigen-presenting cells and on the expression of the interferon-inhibitor UBP43 (Usp18). The replication of IAV correlated with innate immune activation, resulting in IAV eradication. The genetic deletion of Usp18 curbed IAV replication and limited innate immune activation. In conclusion, we found that IAV replicates in SLO, a mechanism which allows innate immune activation.
Highlights
This article is an open access articleAntigen-presenting cells (APC) are major initiators of the innate and adaptive immune response [1,2]
To analyze the role of lymphoid organs during influenza infection without the direct influence of the Influenza A virus (IAV) replication in the lung tissue, we considered that the intravenous infection of IAV would give insights into the capacity of innate immune cells in replicating IAV
About 6 h after systemic infection, IAV was detectable in the spleen (Figure 1a)
Summary
Antigen-presenting cells (APC) are major initiators of the innate and adaptive immune response [1,2]. With their ability to express costimulatory molecules, APCs like dendritic cells (DCs) efficiently prime antigen-specific adaptive immune cells [2,3]. Which supplements antiviral activity in addition to type I interferons (IFN-I) [4,5]. TLR signaling induces IFN-I and results in the maturation and activation of DCs [6,7]. Recent evidence highlights cholesterol metabolism as one major target of IFN-I induced antiviral activity [9]
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