Autophagy Wuhan University Yu Xuejie/Zhou Chuanmin has made important progress in research on neobunia virus transmitted by ticks

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iNature severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging negative-strand enveloped RNA Bunya virus that can cause SFTS with a fatality rate of up to 30%
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Macroautophagy/autophagy is an evolutionarily conserved process that involves maintaining the homeostasis of the host and exhibiting antiviral or pro-viral responses in response to different viral attacks
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However, the interaction between Bunya virus SFTSV and the autophagy process remains largely unclear
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On November 6, 2021, Yu Xuejie and Zhou Chuanmin of Wuhan University published a research paper entitled "Bunyavirus SFTSV exploits autophagic flux for viral assembly and egress" online at Autophagy (IF=16) by a joint communication between Yu Xuejie and Zhou Chuanmin of Wuhan University (Jiamin Yan is the first author of the paper) The study found a new bunya virus-autophagy interaction model.
Bunya virus SFTSV (severe fever with thrombocytopenia syndrome bunyavirus) induces and uses autophagy as its own assembly platform, and buds through autophagy-related vesicles.
Release progeny virus and enhance SFTSV infection
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In summary, the results of this study indicate a new virus-autophagy interaction model, in which Bunyavirus SFTSV induces classic autophagic flux for virus assembly and efflux, indicating that autophagy inhibition may be a treatment or A new therapy that releases SFTS
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Every summer, there is news in the newspapers: "Ticks" bite people to death in a certain place
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Ticks (pí) insects, commonly known as "grass crawlers", are distributed throughout China and are common in woods with grass
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Activities are extremely frequent from April to October
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Ticks are extremely sensitive to carbon dioxide exhaled by humans.
Even if they are more than ten meters away from humans, they can spot the target and approach them quickly
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They will also hibernate on the tips of grass blades for a long time, waiting for the target to pass by and ambush homeopathically.
So far, more than 100 kinds of viruses, bacteria and protozoa have been found in various ticks
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The "new Bunia virus" carried by ticks is extremely deadly and can cause fever with thrombocytopenia syndrome (SFTS).
Its symptoms are mainly fever and thrombocytopenia, accompanied by gastrointestinal reactions.
Severe patients can be caused by multiple organ failure.
For death, the case fatality rate is as high as 30%
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At present, more than 20 provinces in China have reported SFTSV infection, and the number of infections is increasing year by year
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However, it is still not clear about the pathogenic mechanism of SFTSV after infection, and there is a lack of effective vaccines and drugs to prevent, control and treat SFTS
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This study discovered and explored the relationship between SFTSV and autophagy for the first time.
SFTSV infection can activate autophagy, and the autophagy induced by SFTSV depends on its own nuclear protein NP
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SFTSV NP can directly inhibit the interaction between Bcl2 and Beclin1, and induce Beclin1-dependent intact autophagic flux
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Traditionally, it is believed that Bunya virus may assemble in the Golgi apparatus and be released outside the cell through secretory vesicles mediated by the Golgi apparatus.
However, the specific mechanism is still unclear
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This study further evaluated the dynamic interaction process between SFTSV and autophagy after infection, and clarified the dynamic assembly and release process of Bunia virus SFTSV for the first time
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Bunia virus SFTSV relies on the Golgi and the endoplasmic reticulum-Golgi intermediates to form phagophores for assembly.
The assembled progeny SFTSV virus particles can be contained in autophagy-related vesicles (such as autophagosomes and autophagosomes).
Autophagy lysosomes) survive and are directly released outside the cell through the fusion of autophagic vesicles with the cell membrane
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Figure.
Bunia virus SFTSV invasion and release model.
This study reveals for the first time the dynamic process of autophagy in regulating the life cycle of Bunia virus SFTSV, and provides new ideas and new ideas for further understanding of the pathogenic mechanism of SFTSV and the treatment of SFTSV.
The theoretical basis has important scientific significance
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