Immune status in patients with hemorrhagic fever with renal syndrome
Hemorrhagic fever with renal syndrome (HFRS) is a feral herd zoonotic infection caused by hantavirus which manifests with hemorrhages, systemic inflammation, and acute kidney injury (AKI). Many HFRS signs can be explained by their immune nature. Predominantly, immunological changes result from the virus. However, they can be also associated with the damage of vascular endotheliocytes and renal cells targeted by the virus. The aim of this study was to address the role of immune cells in the mechanisms of the immune response in HFRS. It was demonstrated that increased cytotoxic T lymphocytes/CTLs (CD3+CD8+), natural killer T cells (CD3+CD56+), and regulatory T cells (CD3+CD4+FoxP3+ and CD3+CD8+FoxP3) play the key role in the immune response. In contrast to noninfectious AKI, HFRS is associated with less increase in NK T cells but more significant increase in NKG2D expression by CTLs and NK cells. These findings demonstrate that immunological changes are targeted both to eliminate the virus via cytotoxic lymphocytes and to reduce immune mechanisms of cellular damage in HFRS with active involvement of regulatory T cells.