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Host-derived apolipoproteins play comparable roles with viral secretory proteins Ernsand NS1 in the infectious particle formation of Flaviviridae
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نویسنده
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fukuhara t. ,tamura t. ,ono c. ,shiokawa m. ,mori h. ,uemura k. ,yamamoto s. ,kurihara t. ,okamoto t. ,suzuki r. ,yoshii k. ,kurosu t. ,igarashi m. ,aoki h. ,sakoda y. ,matsuura y.
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منبع
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plos pathogens - 2017 - دوره : 13 - شماره : 6
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چکیده
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Amphipathic α-helices of exchangeable apolipoproteins have shown to play crucial roles in the formation of infectious hepatitis c virus (hcv) particles through the interaction with viral particles. among the flaviviridae members,pestivirus and flavivirus possess a viral structural protein ernsor a non-structural protein 1 (ns1) as secretory glycoproteins,respectively,while hepacivirus including hcv has no secretory glycoprotein. in case of pestivirus replication,the c-terminal long amphipathic α-helices of ernsare important for anchoring to viral membrane. here we show that host-derived apolipoproteins play functional roles similar to those of virally encoded ernsand ns1 in the formation of infectious particles. we examined whether ernsand ns1 could compensate for the role of apolipoproteins in particle formation of hcv in apolipoprotein b (apob) and apoe double-knockout huh7 (be-ko),and non-hepatic 293t cells. we found that exogenous expression of either ernsor ns1 rescued infectious particle formation of hcv in the be-ko and 293t cells. in addition,expression of apolipoproteins or ns1 partially rescued the production of infectious pestivirus particles in cells upon electroporation with an erns-deleted non-infectious rna. as with exchangeable apolipoproteins,the c-terminal amphipathic α-helices of ernsplay the functional roles in the formation of infectious hcv or pestivirus particles. these results strongly suggest that the host- and virus-derived secretory glycoproteins have overlapping roles in the viral life cycle of flaviviridae,especially in the maturation of infectious particles,while ernsand ns1 also participate in replication complex formation and viral entry,respectively. considering the abundant hepatic expression and liver-specific propagation of these apolipoproteins,hcv might have evolved to utilize them in the formation of infectious particles through deletion of a secretory viral glycoprotein gene. © 2017 fukuhara et al.
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آدرس
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department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka,japan,laboratory of microbiology,department of disease control,graduate school of veterinary medicine,hokkaido university,hokkaido, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, school of veterinary nursing and technology,faculty of veterinary science,nippon veterinary and life science university,tokyo, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka,japan,laboratory of veterinary microbiology,school of veterinary medicine,kitasato university,aomori, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan, department of virology ii,national institute of infectious diseases,tokyo, Japan, laboratory of public health,department of environmental veterinary sciences,graduate school of veterinary medicine,hokkaido university,hokkaido, Japan, department of virology i,national institute of infectious diseases,tokyo, Japan, global institution for collaborative research and education (gi-core),hokkaido university,hokkaido,japan,division of global epidemiology,research center for zoonosis control,hokkaido university,hokkaido, Japan, school of veterinary nursing and technology,faculty of veterinary science,nippon veterinary and life science university,tokyo, Japan, laboratory of microbiology,department of disease control,graduate school of veterinary medicine,hokkaido university,hokkaido,japan,global institution for collaborative research and education (gi-core),hokkaido university,hokkaido, Japan, department of molecular virology,research institute for microbial diseases,osaka university,osaka, Japan
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Authors
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