HTNV infection induces activation and deficiency of CD8+MAIT cells in HFRS patients

Hantaan virus (HTNV) infection causes an epidemic of hemorrhagic fever with renal syndrome (HFRS) mainly in Asia. Mucosal-associated invariant T (MAIT) cells are innate-like T lymphocytes known to play an important role in innate host defense during virus infection. However, their roles and phenotypes during HTNV infection have not yet been explored. We characterized CD8(+)MAIT cells from HFRS patients based on scRNA-seq data combined with flow cytometry data. We showed that HTNV infection caused the loss and activation of CD8(+)MAIT cells in the peripheral blood, which were correlated with disease severity. The production of granzyme B and IFN-gamma from CD8(+)MAIT cells and the limitation of HTNV replication in endothelia cells indicated the anti-viral property of CD8(+)MAIT cells. In addition, in vitro infection of MAIT cells by HTNV or HTNV-exposed monocytes showed that the activation of MAIT cells was IL-18 mediated. In conclusion, this study identified, for the first time, gene expression profiles of MAIT cells, provided underlying molecular mechanisms for activation of MAIT cells during HTNV infection, and suggested a potential anti-viral role of MAIT cells in HFRS. HTNV infection caused the activation and deficiency of MAIT cells in the peripheral blood. The production of IFN-gamma from MAIT cells can limit the replication of HTNV. The activation of MAIT cells was mediated by IL-18, which was sourced from monocytes infected by HTNV.

Automated summary

This study characterized CD8(+)MAIT cells from HFRS patients using scRNA-seq and flow cytometry. The activation and deficiency of CD8(+)MAIT cells in peripheral blood during HTNV infection were observed, which correlated with disease severity. CD8(+)MAIT cells showed anti-viral properties by producing granzyme B and IFN-gamma, and limiting HTNV replication. The activation of MAIT cells was mediated by IL-18, sourced from HTNV-infected monocytes.