Seminars

Severe fever with thrombocytopenia syndrome (SFTS), a new tick-borne viral disease with a high mortality rate, was first reported in China in 2009, South Korea in 2010, Japan in 2013, Vietnam in 2017, Myanmar in 2018, Taiwan in 2019, and Thailand and Pakistan in 2020.

Most Severe fever with thrombocytopaenia syndrome virus (SFTSV, officially named Dabie bandavirus) infections occur via bites from the tick Haemaphysalis longicornis; however, SFTSV transmission can also occur through close contact with an infected patient and animals like cat and dog.

SFTSV can cause severe and often fatal disease characterized by hyperinflammation and a cytokine storm with rapid and prolonged systemic elevation of interleukin 10 (IL-10) and IL-6 and we reported that systemic hyperproduction of both IL-10 and IL-6 and low systemic production of transforming growth factor‐β (TGF-β) can generate a cytokine storm in fatal SFTS and severe and critical coronavirus disease 2019 (COVID-19) and suggested that IL-10 may play a pathological role in the severity of SFTS and COVID-19.

Macrophages are the major innate immune cells involved in infection and inflammation and are the first line of defence against SFTSV and SARS-CoV-2 infection. Macrophage activation syndrome (MAS), a form of cytokine release syndrome (CRS), also known as a cytokine storm, is observed in patients with fatal SFTS and severe and critical COVID-19.

Therefore, we studied the phenotypes of macrophages in patients with SFTS ranging in severity from mild to fatal and found that the population of HLA-DR⁺CD86⁺macrophages was increased and the population of CD163⁺CD206⁺macrophages was decreased in patients with fatal SFTS.

When we blocked IL‐10 signalling using antibodies against the IL‐10 receptor in vitro in human macrophage cells under different conditions-SFTSV-, SARS-CoV-2- infection, and LPS induction and found that antibodies against the IL‐10 receptor can reduce IL‐6 and tumour necrosis factor (TNF-α) production and increase TGF‐β production in SFTSV- and SARS‐CoV‐2‐infected and LPS‐induced human macrophage cells.

Therefore, we suggest that IL-10 could serve as a prognostic target and antibodies against the IL-10 receptor is a potential immune-based intervention against fatal SFTS and critical COVID-19.