Evidence map›Paper›PMID 33534867›Full record

ArticlePLoS pathogens2021

A highly attenuated vaccinia virus strain LC16m8-based vaccine for severe fever with thrombocytopenia syndrome.

Tomoki Yoshikawa, Satoshi Taniguchi, Hirofumi Kato, Naoko Iwata-Yoshikawa, Hideki Tani, Takeshi Kurosu, Hikaru Fujii, Natsumi Omura, Miho Shibamura, Shumpei Watanabe and 11 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 3 institutions in 1 country.

Tomoki YoshikawaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.ORCID 0000-0001-7601-4036
Satoshi TaniguchiDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.ORCID 0000-0002-2066-1979
Hirofumi KatoDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Naoko Iwata-YoshikawaDepartment of Pathology, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Hideki TaniDepartment of Virology, Toyama Institute of Health, Imizu-shi, Toyama, Japan.
Takeshi KurosuDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Hikaru FujiiDepartment of Microbiology, Faculty of Veterinary Medicine, Okayama University of Science, Imabari-shi, Ehime, Japan.
Natsumi OmuraDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Miho ShibamuraDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.ORCID 0000-0002-1600-6242
Shumpei WatanabeDepartment of Microbiology, Faculty of Veterinary Medicine, Okayama University of Science, Imabari-shi, Ehime, Japan.ORCID 0000-0003-3359-7192
Kazutaka EgawaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Takuya InagakiDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Satoko SugimotoDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Supranee PhanthanawiboonDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Shizuko HaradaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Souichi YamadaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.ORCID 0000-0001-7183-7818
Shuetsu FukushiDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Shigeru MorikawaDepartment of Microbiology, Faculty of Veterinary Medicine, Okayama University of Science, Imabari-shi, Ehime, Japan.
Noriyo NagataDepartment of Pathology, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
Masayuki ShimojimaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.ORCID 0000-0002-5745-8413
Masayuki SaijoDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama-shi, Tokyo, Japan.
National Institute of Infectious Diseases · JPOkayama University of Science · JPToyama Institute of Health · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe fever with thrombocytopenia syndrome (SFTS) caused by a species Dabie bandavirus (formerly SFTS virus [SFTSV]) is an emerging hemorrhagic infectious disease with a high case-fatality rate. One of the best strategies for preventing SFTS is to develop a vaccine, which is expected to induce both humoral and cellular immunity. We applied a highly attenuated but still immunogenic vaccinia virus strain LC16m8 (m8) as a recombinant vaccine for SFTS. Recombinant m8s expressing SFTSV nucleoprotein (m8-N), envelope glycoprotein precursor (m8-GPC), and both N and GPC (m8-N+GPC) in the infected cells were generated. Both m8-GPC- and m8-N+GPC-infected cells were confirmed to produce SFTSV-like-particles (VLP) in vitro, and the N was incorporated in the VLP produced by the infection of cells with m8-N+GPC. Specific antibodies to SFTSV were induced in mice inoculated with each of the recombinant m8s, and the mice were fully protected from lethal challenge with SFTSV at both 103 TCID50 and 105 TCID50. In mice that had been immunized with vaccinia virus strain Lister in advance of m8-based SFTSV vaccine inoculation, protective immunity against the SFTSV challenge was also conferred. The pathological analysis revealed that mice immunized with m8-GPC or m8-N+GPC did not show any histopathological changes without any viral antigen-positive cells, whereas the control mice showed focal necrosis with inflammatory infiltration with SFTSV antigen-positive cells in tissues after SFTSV challenge. The passive serum transfer experiments revealed that sera collected from mice inoculated with m8-GPC or m8-N+GPC but not with m8-N conferred protective immunity against lethal SFTSV challenge in naïve mice. On the other hand, the depletion of CD8-positive cells in vivo did not abrogate the protective immunity conferred by m8-based SFTSV vaccines. Based on these results, the recombinant m8-GPC and m8-N+GPC were considered promising vaccine candidates for SFTS.

Indexed as

AnimalsAntigens, ViralFemaleMaleMiceMice, Inbred C57BLNucleoproteinsPhlebovirusSevere Fever with Thrombocytopenia SyndromeVaccines, AttenuatedVaccines, SyntheticViral Envelope ProteinsAntigens, ViralNucleoproteinsVaccines, AttenuatedVaccines, SyntheticViral Envelope Proteins

Identifiers

PMID33534867
PMCPMC7886154
OpenAlexW3127770131

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.