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    Home > Biochemistry News > Biotechnology News > The dynamic process of SFTSV invading host cells and releasing them in cytoplasm is revealed.

    The dynamic process of SFTSV invading host cells and releasing them in cytoplasm is revealed.

    • Last Update: 2020-08-06
    • Source: Internet
    • Author: User
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    Fever with platelet reduction syndrome virus (SFTSV) is a new type of Bunia virus found in China in recent years, and its fatality rate is as high as 30%.
    , the infection and pathogenic mechanisms of SFTSV are not clear, and there is a lack of effective vaccines and drugs for the prevention and treatment of related diseases.
    invasion is the first key step in viral infection and a target for many antiviral drug designs.
    lackof further research into the invasion of Bunia virus.
    a joint team of researchers from Huazhong University of Science and Technology and wuhan virus research institute of the Chinese Academy of Sciences systematically revealed for the first time the dynamic processofs of SFTSV invading host cells and releasing in cytoplasm using single-particle tracing technology based on quantum slot markers and multicolor imaging.
    study found that SFTSV infection can recruit the mesh protein in the cytoplasm to be assembled on the cytoplasm membrane, forming the mesh protein packet seamount (clathrin-coated pits, CCPs), and then, under the action of the dynamic protein (dynamin), the CCP wraps the virus particles from the membrane to form a complete mesh protein pack (clathrin-coated vecess.
    virus with the inner swallowing of small bubbles into the cytoplasm, CCV surface package of the mesh protein gradually dissoced, the virus particles are presented into the early endothelial, and then into the late endosome.
    virus relies on micro-wire for cytoskeleton transport near cytoplasmic membranes, while microcells are transported mainly within cytoplasm.
    finally, the viral particles in the late end of the internal acid environment triggered by (-pH5.6) and the endoscosphrium membrane fusion, release nucleic acid, complete the entire invasion process.
    this study systematically and visually reveals the dynamic process of SFTSV intrusion and the interaction of the virus espertin involved in it, which lays the foundation for the interpretation of SFTSV infection mechanism and the prevention and treatment of fever-related platelet reduction syndrome.
    related research Single-Particle Reveals The Mail Entry Process of the Bunyavirus Severe Fever with Thrombocytopenia Syndrome Virus has been published online in the journal Small. Liu Jia, a postdoctoral fellow at Huazhong University of Science and Technology in
    , is the first author of the paper, and Zhou Yiwu, a professor at Tongji Medical College of Huazhong University of Science and Technology, and Wang Manli, an associate researcher at the Wuhan Virus Institute of the Chinese Academy of Sciences, are co-authors of the paper.
    received strong support from The Team of Professor Pang Daiwen of Wuhan University during the project research process.
    the research was supported by the NSFC Innovation Group Project (31621061) and key projects (21535005), special funds for basic scientific research business expenses of central universities (2016 JCTD117), and the National Key Laboratory Open Fund for Virology (2017 IOV007). Wu Zhiwei's team at Nanjing University in
    found that severe fever accompanied by platelet reduction (SFTS) was a new infectious disease caused by a new type of virus and associated with high mortality rate.
    lack of treatment interventions, the pathogenesis of the disease has not yet been fully clarified.
    Although there have been relevant studies in antiviral immune response, little is known about the body fluid participation of the pathogenesis of the virus.
    August 20, 2018, Wu Zhiwei of Nanjing University School of Medicine published an article entitled "Deficient humoral responses and disrupted B-celli are eisedwithd with fatal SFTSV infection" at Nature Communications.
    study revealed the significant effects of b-cell immunity on fever-associated platelet reduction due to lack of body fluid response and destruction.
    severe fever with platelet reduction (SFTS) is an emerging infectious disease caused by a new type of virus, Bunia virus.
    increasing sFTSV infections have attracted close attention in East Asia.
    the mortality rate of SFTSV infection in this region ranged from 10% to 30%, significantly higher than haemorrhagic fever caused by the Hantan virus in the same area.
    Although the virus is mainly transmitted through tick bites, studies have confirmed that it can be transmitted through humans.
    there is no effective treatment or vaccine, the pathogenesis of the disease is not clear.
    Although previous studies have shown that the impairment of congenital immune response and inflammatory cytokines play an important role in disease progression, our knowledge of the viral-specific body fluid response of SFTSV infection and its role in the pathogenesis is still very limited.
    B-cell-dependent immunogenic presentation cells (APC) and follicle-assisted T cells (Tfh) regulation.
    previous studies have shown that a single dendritic cell (DC) restrictive antigen presentation can initiate the Tfh cell program, but not the final effect differentiation.
    However, the synergy of MHC-II-positive DCs and B cells can achieve the best results for viral infection seisiating of Tfh and Bioccentre (GC) B cells.
    Tfh, together with the foeliad DC, repeatedly interacts with the B cells experienced by the antigen in GC repeatedly, promoting the amplification of B cells in the mother cell and memory B cells, differentiation and affinity maturation to produce high affinity antibodies.
    , Tfh, which resides mainly on the lymph nodes (LN) and spleen (SP) GC, plays a key role in pathogen-specific category conversion and antibody production.
    many early studies have shown that peripheral Tfh (pTfh) cells exhibit similarities to transcription and phenotype of lymphatic Tfh cells.
    the experiment studied the regulatory status of Tfh in peripheral blood in SFTS patients.
    in addition to the homologous interactions between immune cells, it is also necessary to regulate cytokines such as IL-4, GM-CSF, IL-21, and IL-6 to produce and maintain neutralizing antibody responses.
    in human-derived mouse models with immature B cells and lack of CD209 plus (DC-SIGN) human DCs, human GM-CSF and IL-4 expressions can correct IgG's reaction defects against primary stimulation 15.
    in addition, IL-4 and IL-21 have been shown to be the basic effects of Tfh cells in the Th2 body fluid reaction 16.
    IL-21 has been shown to be a key marker for Tfh cells in phenotypes and functions.
    interesting, IL-6 is an ephymatic sphysic factor that is essential for gradually increasing cellular reactions to control persistent viral infections.
    however, the role of these cytokines in the body fluid response of SFTSV infection is poorly known.
    recent studies have shown that SFTSV effectively infects mononucleic cells and interferes with the signaling pathways of innate immunity, thereby affecting adaptive immune responses.
    also showed that SFTSV infection hindered the differentiation of bone marrow DCs8.
    considering the importance of APC in establishing adaptive immune responses, the study hypothesized defects in body fluid responses caused by SFTSV infections.
    in the current study of patient quealities, the researchers examined the dynamic properties of serological responses, regulated B-cell subgroups, bone marrow DC (mDCs) and pTfh cells, as well as several associated regulatory cytokines, and clarified the state of B-cell-dependent immunological response and its role in the pathogenesis of this pathogenic viral infection.
    the results of the study, The defective seroological response of SFTSV is associated with disease mortality, and the combination of B-cell and T-cell damage helps to destroy antiviral immunity. the serological characteristics of
    deceased patients are characterized by the absence of specific IgG for viral nucleocases and glycoproteins due to the failure of B-cell type conversion.
    antibody secretion amplification and damage is a sign of fatal SFTSV infection. The apoptosis of
    early infection of mononucleoblasts reduced the antigen presentation of dendritic cells, hindered the differentiation and function of T-bubble-assisted cells, and led to the failure of viral-specific body fluid response.
    Source: Wuhan Virus Research Institute, glucocorticoids.
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