The Endless Wars: Severe Fever With Thrombocytopenia Syndrome Virus, Host Immune and Genetic Factors

Abstract

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging arboviral infectious disease with a high rate of lethality in susceptible humans and caused by severe fever with thrombocytopenia syndrome bunyavirus (SFTSV). Currently, neither vaccine nor specific antiviral drugs are available. In recent years, given the fact that both the number of SFTS cases and epidemic regions are increasing year by year, SFTS has become a public health problem. SFTSV can be internalized into host cells through the interaction between SFTSV glycoproteins and cell receptors and can activate the host immune system to trigger antiviral immune response. However, SFTSV has evolved multiple strategies to manipulate host factors to create an optimal environment for itself. Not to be discounted, host genetic factors may be operative also in the never-ending winning or losing wars. Therefore, the identifications of SFTSV, host immune and genetic factors, and their interactions are critical for understanding the pathogenic mechanisms of SFTSV infection. This review summarizes the updated pathogenesis of SFTS with regard to virus, host immune response, and host genetic factors to provide some novel perspectives of the prevention, treatment, as well as drug and vaccine developments.

Severe fever with thrombocytopenia syndrome virus trends and hotspots in clinical research: A bibliometric analysis of global research

“…Severe fever with thrombocytopenia syndrome (SFTS) virus (SFTSV) is a type of Bunyavirus that is seemingly transmitted by ticks, such as Haemaphystick longicornis ( 1 , 2 ). A significant number of SFTSV are human pathogens that can cause severe diseases such as hepatitis, encephalitis, and hemorrhagic fever ( 3 ). SFTSV was firstly detected in 2009 in rural parts of central and northeastern China ( 4 ).…”

“…In 2015, the fatality rate for SFTS in Japan and South Korea was over 30% ( 9 ). SFTSV can evolve rapidly through genetic mutations and has already become a major threat to public health ( 3 ). There is no specific treatment for SFTSV, and the only method to prevent SFTSV infection and transmission is to avoid tick bites ( 10 ).…”

Evaluation of reverse transcription loop‐mediated isothermal amplification assay for the detection of severe fever with thrombocytopenia syndrome in clinical laboratories: A single‐center study

“…The virus is a spherical virion that comprises three RNA segments: large (L), medium (M), and small (S). The main clinical manifestations of SFTS include fever, thrombocytopenia, leukopenia, vomiting, and diarrhea, and it can even cause multiorgan failure with a high fatality rate (approximately 5%–30%) 1–4 . Based on the disease presentation, the clinical course of SFTS infection can be divided into four phases: incubation, acute, multiple organ failure, and recovery phases 5 .…”

“…7 Most patients with severe SFTS experience multiple organ dysfunction, shock, diffuse intravascular coagulation, and eventually, death. 2,8 To the best of knowledge, effective anti-SFTSV interventions are not currently available. After the detection of its first case in China in 2009, the number of SFTS endemic areas has gradually increased to more than seven countries in East Asia, including China, Vietnam, South Korea, Pakistan, Myanmar, Thailand, and Japan.…”

“…The main clinical manifestations of SFTS include fever, thrombocytopenia, leukopenia, vomiting, and diarrhea, and it can even cause multiorgan failure with a high fatality rate (approximately 5%-30%). [1][2][3][4] Based on the disease presentation, the clinical course of SFTS infection can be divided into four phases: incubation, acute, multiple organ failure, and recovery phases. 5 Previous studies have shown that during the acute phase, patients with confirmed SFTS infection have a high viral load in their serum, which is associated with their prognosis.…”