Antiviral immunity of severe fever with thrombocytopenia syndrome: current understanding and implications for clinical treatment

Abstract

Dabie Banda virus (DBV), a tick-borne pathogen, was first identified in China in 2009 and causes profound symptoms including fever, leukopenia, thrombocytopenia and multi-organ dysfunction, which is known as severe fever with thrombocytopenia syndrome (SFTS). In the last decade, global incidence and mortality of SFTS increased significantly, especially in East Asia. Though previous studies provide understandings of clinical and immunological characteristics of SFTS development, comprehensive insight of antiviral immunity response is still lacking. Here, we intensively discuss the antiviral immune response after DBV infection by integrating previous ex- and in-vivo studies, including innate and adaptive immune responses, anti-viral immune responses and long-term immune characters. A comprehensive overview of potential immune targets for clinical trials is provided as well. However, development of novel strategies for improving the prognosis of the disease remains on challenge. The current review may shed light on the establishment of immunological interventions for the critical disease SFTS.

Keywords: SFTS; antiviral immunity; clinical treatment; immune cells; immune response.

Figure 1

(A) The virus attaches to the surface of host cells, and subsequently enters cells. Low pH triggers the fusion of the virus with the cell membrane and releases the viral ribonucleic protein complex into the cytoplasm. (B) NSs of DBV can hinder the production and response of intracellular IFN by encapsulating the STAT heterodimer and TBK1/IKKϵ, and block the phosphorylation of STAT2 and nuclear translocation of STAT, ultimately leading to a complete blockade of the IFN response.

Figure 2

Antiviral immunity and patient prognosis of SFTS.