Immune Cells at the Frontline of SFTSV Infection.

Area of Science:

• Virology
• Immunology
• Pathogenesis

Background:

• Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne virus causing hemorrhagic fever.
• Existing research lacks an integrated framework linking SFTSV immune cell tropism to disease pathogenesis.
• SFTSV exhibits broad immune cell tropism, impacting monocytes, B cells, T cells, dendritic cells, NK cells, and macrophages.

Purpose of the Study:

• To synthesize the roles and functional features of immune cells in SFTSV pathogenesis.
• To integrate clinical, experimental, and molecular evidence on SFTSV infection.
• To highlight advances in host-directed immunotherapies for SFTSV.

Main Methods:

• Review of clinical, experimental, and molecular studies on SFTSV.
• Analysis of viral immune cell tropism and its impact on immune responses.
• Examination of viral protein NSs's role in antagonizing host interferon signaling.

Main Results:

• SFTSV infects monocytes and B cells, serving as viral reservoirs and cytokine sources, impairing B cell antibody production.
• T cells exhibit depletion and exhaustion; dendritic cells lose antigen-presenting capacity.
• NSs protein suppresses type I and II interferon responses by interfering with host signaling pathways.

Conclusions:

• Immune cell tropism and dysfunction are central to SFTSV pathogenesis.
• Understanding immune cell roles is crucial for developing effective SFTSV treatments.
• Host-directed immunotherapies offer promising avenues for managing SFTSV infection.