An emerging hemorrhagic fever in China caused by a novel bunyavirus SFTSV

Zhang, XiaoShuang S.; Liu, Yan; Zhao, Li; Li, Bing; Yu, Hao; Wen, Hongling; Yu, Xue Jie

doi:10.1007/s11427-013-4518-9

Cited by 71 publications

(58 citation statements)

References 25 publications

(49 reference statements)

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“…Such knowledge will be useful for developing antivirals against SFTSV and other pathogenic phleboviruses. Until recently, the SFTSV was considered a member of the Bunyaviridae family, genus Phlebovirus (1,33,35). Following a recent proposal to the International Committee on the Taxonomy of Viruses, the Bunyaviridae family was reclassified as the Bunyavirales order, and SFTSV now belongs to the Phenuiviridae family (1).…”

Section: Methodsmentioning

confidence: 99%

Targeting of severe fever with thrombocytopenia syndrome virus structural proteins to the ERGIC (endoplasmic reticulum Golgi intermediate compartment) and Golgi complex

et al. 2018

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Severe fever with thrombocytopenia syndrome phlebovirus (SFTSV) is a newly emerged phlebovirus identified in China, Japan, and South Korea. Phlebovirus glycoproteins (GP) play a key role in targeting viral structural components to the budding compartments in the ER-Golgi intermediate compartment (ERGIC) and Golgi complex. However, the role of SFTSV GP in targeting structural proteins to the ERGIC and Golgi complex remains unresolved. In this study, we show that SFTSV GP plays a significant role in targeting RNA-dependent RNA polymerase (L) and nucleocapsid protein (NP) to the budding sites. Confocal microscopy was used to investigate the subcellular localization of SFTSV structural proteins. In SFTSV-infected cells, GP and L localized to the ER, ERGIC and Golgi complex, whereas NP localized to the ERGIC and Golgi complex. In addition, GP colocalized with L and NP in infected cells. In cells singly transfected with GP, L or NP, GP localized to the same subcellular compartments as in infected cells. However, L or NP alone did not localize to the ER, ERGIC, or Golgi complex. Cotransfection experiments showed that GP altered the localization of L to the ERGIC and Golgi complex but not that of NP. Interestingly, plasmid-expressed NP fused with a hemagglutinin tag localized to the ERGIC and Golgi complex when expressed in SFTSV-infected cells and colocalised with GP, suggesting that GP plays a role in the subcellular localization of L and NP in infected cells. Thus, the SFTSV structural components start to assemble at the ERGIC to Golgi complex. GP is required for transporting L and NP to the ERGIC and Golgi complex. In addition, targeting of NP requires interaction with other factors besides GP.

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Section: Methodsmentioning

confidence: 99%

Targeting of severe fever with thrombocytopenia syndrome virus structural proteins to the ERGIC (endoplasmic reticulum Golgi intermediate compartment) and Golgi complex

et al. 2018

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“…Among a total of 2,047 cases recorded nationally in 2011 and 2012, 625 cases were reported from the Xinyang region in Henan Province, the most heavily affected area in China. 5,6 Until recently, seroprevalence of the SFTSV antibody in local residents was not analyzed in light of temporal, population, and spatial distribution.…”

Section: Introductionmentioning

confidence: 99%

The Severe Fever with Thrombocytopenia Syndrome Bunyavirus (SFTSV) Antibody in a Highly Endemic Region from 2011 to 2013: A Comparative Serological Study

Hu¹,

Guo²,

Yang³

et al. 2015

The American Society of Tropical Medicine and Hygiene

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“…4A. Briefly, due to the possibility that the virions and extracellular vesicles may have similar sizes and densities and that our procedure would not completely devoid the extracellular vesicles from free virions (28,38), we carried out an immune-selection step using anti-CD63 beads (Fig. 6A) as previously described (39), followed by a second immune(-negative) selection using magnetic beads coated with antibodies against SFTS virus (Fig.…”

Section: Sfts Virus Infection Induces the Formation Of Cytoplasmic Stmentioning

confidence: 99%

Extracellular Vesicles Mediate Receptor-Independent Transmission of Novel Tick-Borne Bunyavirus

Silvas

Popov

Paulucci-Holthauzen

et al. 2016

J Virol

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Severe fever with thrombocytopenia syndrome (SFTS) virus is a newly recognized member of the genus Phlebovirus in the family Bunyaviridae. The virus was isolated from patients presenting with hemorrhagic manifestations and an initial case fatality rate of 12 to 30% was reported. Due to the recent emergence of this pathogen, there is limited knowledge on the molecular virology of SFTS virus. Recently, we reported that the SFTS virus NSs protein inhibited the activation of the beta interferon (IFN-␤) promoter. Furthermore, we also found that SFTS virus NSs relocalizes key components of the IFN response into NSs-induced cytoplasmic structures. Due to the important role these structures play during SFTS virus replication, we conducted live cell imaging studies to gain further insight into the role and trafficking of these cytoplasmic structures during virus infection. We found that some of the SFTS virus NSs-positive cytoplasmic structures were secreted to the extracellular space and endocytosed by neighboring cells. We also found that these secreted structures isolated from NSs-expressing cells and SFTS virus-infected cells were positive for the viral protein NSs and the host protein CD63, a protein associated with extracellular vesicles. Electron microscopy studies also revealed that the isolated CD63-immunoprecipitated extracellular vesicles produced during SFTS virus infection contained virions. The virions harbored within these structures were efficiently delivered to uninfected cells and were able to sustain SFTS virus replication. Altogether, these results suggest that SFTS virus exploits extracellular vesicles to mediate virus receptor-independent transmission to host cells and open the avenue for novel therapeutic strategies against SFTS virus and related pathogens. IMPORTANCESFTS virus is novel bunyavirus associated with hemorrhagic fever illness. Currently, limited information is available about SFTS virus. In the present study, we demonstrated that extracellular vesicles produced by SFTS virus-infected cells harbor infectious virions. We sought to determine whether these "infectious" extracellular vesicles can mediate transmission of the virus and confirmed that the SFTS virions were efficiently transported by these secreted structures into uninfected cells and were able to sustain efficient replication of SFTS virus. These results have significant impact on our understanding of how the novel tick-borne phleboviruses hijack cellular machineries to establish infection and point toward a novel mechanism for virus replication among arthropod-borne viruses. The Bunyaviridae family comprises five genera, including Orthobunyavirus, Phlebovirus, Nairovirus, Hantavirus, and Tospovirus. The majority of viruses within this family (with the exception of Hantaviruses) are considered arthropod-borne viruses and are important causes of morbidity and mortality around the world. These viruses are associated with a range of clinical symptoms characterized by febrile illness and in the most severe cases fatal hepa...

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An emerging hemorrhagic fever in China caused by a novel bunyavirus SFTSV

Cited by 71 publications

References 25 publications

<b>Targeting of severe fever with thrombocytopenia syndrome virus structural proteins to the ERGIC (endoplasmic reticulum Golgi intermediate compartment) and Golgi </b><b>complex </b>

<b>Targeting of severe fever with thrombocytopenia syndrome virus structural proteins to the ERGIC (endoplasmic reticulum Golgi intermediate compartment) and Golgi </b><b>complex </b>

The Severe Fever with Thrombocytopenia Syndrome Bunyavirus (SFTSV) Antibody in a Highly Endemic Region from 2011 to 2013: A Comparative Serological Study

Extracellular Vesicles Mediate Receptor-Independent Transmission of Novel Tick-Borne Bunyavirus

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