# Immune Cells at the Frontline of SFTSV Infection

## TL;DR

This paper reviews how immune cells respond to SFTSV infection and how the virus disrupts immune defenses, leading to severe disease.

## Contribution

The paper integrates clinical, experimental, and molecular evidence to clarify immune cell roles in SFTSV pathogenesis.

## Key findings

- Monocytes and B cells are major viral reservoirs and sources of inflammation during SFTSV infection.
- T cells and dendritic cells show functional impairments in severe SFTSV cases.
- The viral NSs protein disrupts interferon signaling by sequestering key host proteins.

## Abstract

Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne Dabie bandavirus that causes hemorrhagic fever with high case fatality. Although numerous studies have examined specific aspects of SFTSV infection, an integrated framework that links viral immune cell tropism to immunopathogenesis remains lacking. The virus exhibits broad immune tropism, particularly infecting monocytes and B cells, which serve as major viral reservoirs and sources of inflammatory cytokines, while B cells additionally show impaired antibody production. T cells undergo numerical depletion and functional exhaustion, and dendritic cells lose antigen-presenting capacity in severe cases. Natural killer cells and macrophages also exhibit altered activation and polarization, contributing to both antiviral defense and immunopathology. A key viral protein, NSs, antagonizes host interferon signaling by sequestering TBK1, IRF3, and STAT1/2 into viral inclusion bodies, thereby suppressing type I and II IFN responses. Murine models with disrupted IFNAR signaling have been widely used to study SFTSV pathogenesis in vivo. In this review, we aim to integrate clinical, experimental, and molecular evidence to synthesize the roles and functional features of immune cells underlying SFTSV pathogenesis and highlight host-directed immunotherapeutic advances.