Host Cell Factors Involved in Filovirus Infection

Kajihara, Masahiro; Takada, Ayato

doi:10.1007/s40475-015-0039-x

Cited by 2 publications

(2 citation statements)

References 125 publications

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“…RESTV has never caused lethal infection in humans. Filoviruses infect a variety of cell types in vitro [ 1 – 6 ], and several cellular factors have been shown to be involved in filovirus replication in host cells [ 7 , 8 ]. However, the details of the mechanisms underlying the cell tropism and pathogenicity of filoviruses have not been fully elucidated yet.…”

Section: Introductionmentioning

confidence: 99%

Putative endogenous filovirus VP35-like protein potentially functions as an IFN antagonist but not a polymerase cofactor

et al. 2017

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It has been proposed that some non-retroviral RNA virus genes are integrated into vertebrate genomes. Endogenous filovirus-like elements (EFLs) have been discovered in some mammalian genomes. However, their potential roles in ebolavirus infection are unclear. A filovirus VP35-like element (mlEFL35) is found in the little brown bat (Myotis lucifugus) genome. Putative mlEFL35-derived protein (mlEFL35p) contains nearly full-length amino acid sequences corresponding to ebolavirus VP35. Ebola virus VP35 has been shown to bind double-stranded RNA, leading to inhibition of type I interferon (IFN) production, and is also known as a viral polymerase cofactor that is essential for viral RNA transcription/replication. In this study, we transiently expressed mlEFL35p in human kidney cells and investigated its biological functions. We first found that mlEFL35p was coimmunoprecipitated with itself and ebolavirus VP35s but not with the viral nucleoprotein. Then the biological functions of mlEFL35p were analyzed by comparing it to ebolavirus VP35s. We found that the expression of mlEFL35p significantly inhibited human IFN-β promoter activity as well as VP35s. By contrast, expression of mlEFL35p did not support viral RNA transcription/replication and indeed slightly decrease the reporter gene expression in a minigenome assay. These results suggest that mlEFL35p potentially acts as an IFN antagonist but not a polymerase cofactor.

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Section: Introductionmentioning

confidence: 99%

Putative endogenous filovirus VP35-like protein potentially functions as an IFN antagonist but not a polymerase cofactor

et al. 2017

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“…Filoviruses are known to cause fulminant hemorrhagic fevers in humans with case-fatality rates up to 90% [23,25]. MARV was the first filovirus discovered in 1967 during lab outbreaks in Marburg, Germany and Yugoslavia transmitted to humans from infected monkeys imported from Uganda.…”

Section: Historymentioning

confidence: 99%

Comparison of antibody responses in mice generated by different multivalent Filovirus vaccines based on recombinant glycoprotein subunits

Tashiro¹

2020

The Journal of Immunology

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Filoviruses cause fulminant hemorrhagic fevers with case-fatality rates up to 90%. Recombinant glycoprotein (GP) derived from Ebola virus (EBOV), Sudan virus (SUDV) and Marburg virus (MARV) have been expressed from stably transformed Drosophila S2 cells and used to formulate recombinant subunit vaccine candidates showing efficacy in rodents and non-human primates. Immunogenicity of 11 different formulations of our trivalent subunit vaccine with adjuvant was tested. Each group of Swiss Webster mice was administered a formulation with or without adjuvant. Mouse sera were collected two weeks after 2nd and 3rd vaccine doses and diluted 1:8,000 and 1:40,000 to determine titers of IgG binding to EBOV, SUDV and MARV GP by a microsphere immunoassay (MIA). MFI (median fluorescence intensity) was collected by Luminex xPonent software then graphed and statistically analyzed using GraphPad Prism. As expected, groups administered equal amounts of EBOV, SUDV, and MARV GP had the most balanced antibody response as compared to groups that did not receive equal amounts of GP. Formulations with optimal antigen doses generate balanced antigen-binding antibody responses. Additional experiments are ongoing including the characterization of virus neutralization activity of the different formulations.

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Host Cell Factors Involved in Filovirus Infection

Cited by 2 publications

References 125 publications

Putative endogenous filovirus VP35-like protein potentially functions as an IFN antagonist but not a polymerase cofactor

Putative endogenous filovirus VP35-like protein potentially functions as an IFN antagonist but not a polymerase cofactor

Comparison of antibody responses in mice generated by different multivalent Filovirus vaccines based on recombinant glycoprotein subunits

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