tetano
Editor, Senior Moderator
Pathogens
. 2021 May 19;10(5):622.
doi: 10.3390/pathogens10050622.
Replication of Influenza A Virus in Secondary Lymphatic Tissue Contributes to Innate Immune Activation
Sarah-Kim Friedrich[SUP] 1 [/SUP], Rosa Schmitz[SUP] 1 [/SUP], Michael Bergerhausen[SUP] 1 [/SUP], Judith Lang[SUP] 1 [/SUP], Vikas Duhan[SUP] 1 [/SUP], Cornelia Hardt[SUP] 1 [/SUP], Matthias Tenbusch[SUP] 2 [/SUP], Marco Prinz[SUP] 3 4 5 6 [/SUP], Kenichi Asano[SUP] 7 [/SUP], Hilal Bhat[SUP] 1 8 [/SUP], Thamer A Hamdan[SUP] 1 9 [/SUP], Philipp Alexander Lang[SUP] 10 [/SUP], Karl Sebastian Lang[SUP] 1 [/SUP]
Affiliations
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.
Keywords: Influenza virus; enforced viral replication; innate immune activation.
. 2021 May 19;10(5):622.
doi: 10.3390/pathogens10050622.
Replication of Influenza A Virus in Secondary Lymphatic Tissue Contributes to Innate Immune Activation
Sarah-Kim Friedrich[SUP] 1 [/SUP], Rosa Schmitz[SUP] 1 [/SUP], Michael Bergerhausen[SUP] 1 [/SUP], Judith Lang[SUP] 1 [/SUP], Vikas Duhan[SUP] 1 [/SUP], Cornelia Hardt[SUP] 1 [/SUP], Matthias Tenbusch[SUP] 2 [/SUP], Marco Prinz[SUP] 3 4 5 6 [/SUP], Kenichi Asano[SUP] 7 [/SUP], Hilal Bhat[SUP] 1 8 [/SUP], Thamer A Hamdan[SUP] 1 9 [/SUP], Philipp Alexander Lang[SUP] 10 [/SUP], Karl Sebastian Lang[SUP] 1 [/SUP]
Affiliations
- PMID: 34069514
- DOI: 10.3390/pathogens10050622
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.
Keywords: Influenza virus; enforced viral replication; innate immune activation.