A Newly Discovered Severe Fever with Thrombocytopenia Syndrome Virus and its Mechanisms in Evading Host Innate Immunity
Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly found virus that causes severe fever and thrombocytopenia. There is no specific treatment for SFTSV infection, although researches have been focusing on studying the pathogenic mechanisms of SFTSV. It has been shown that TBK1/IKKε plays an important role in IFN induction. Interestingly, the S segment of SFTSV genome encodes nonstructural protein (NSs) that can induce inclusion bodies (IBs) formation to isolate the kinases from mitochondrial platform to evade host innate immunity. As a result, interactions between NSs of SFTSV and TBK1/IKKε pathway become a hot topic to pursue new antiviral drugs against this virus. Furthermore, glycoprotein Gn/Gc encoded by the M segment could meditate virus entry into host cells, which may become a target for neutralizing antibody.
SFTSV is newly discovered virus that was first reported in China dated back to 2009. The virus was also reported in some other countries, such as in Japan, Korea and USA. Until now, there is no effective vaccine to prevent this disease, and the efficacy of traditional antiviral treatment needs improving. As a result, many labs have been focusing on studying the molecular mechanisms of pathogenesis of SFTSV in order to find the targets for antiviral drug intervention and vaccine development. One example comes from NSs of SFTSV, due to the fact that it can meditate IBs information and IBs can irreversibly spatial isolateTBK1/IKKε from mitochondrial antiviral platform. But there is no report about TBK1/IKKε signaling at other subcellular sites which can be prevented by the spatial isolation of IBs as well. Many scientists now concentrate on the research of NSs inhibitors which may be a hot spot in the future. The M segment encoded glycoprotein Gn/Gc is also a target for research. The glycoprotein entry into the envelope of the virus, and combines the cell receptor, promotes virus entry into the host cells, and the C-type lectin DC-SIGN was found to serve as a receptor for SFTSV Gn/Gc-driven entry into cell lines and dendritic cells. But Monocytic (THP-1) cells, HFF, and cervical carcinoma (HeLa) cells were resistant to SFTSV Gn/Gc-driven entry, indicating that these cells lack expression of the appropriate receptor(s). So Gn/Gc could be a target for neutralizing antibodies on one way and it may also become a hot spot for the research of antiviral drugs on the other way. Under current condition, we should concentrate on the prevention of this disease; keep away from each route of transmission and more in depth study on the molecular mechanisms of viral pathogenesis for more effective antiviral drug intervention.