Evidence map›Paper›PMID 41190813›Full record

ArticleJournal of virology2025

CD36 is required for human sapovirus propagation.

Tomoichiro Oka, Yuko Okemoto-Nakamura, Hirotaka Takagi

Abstract read
In one paragraph

Article in Journal of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
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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

3 authors.

Tomoichiro Oka *Department of Virology II, Japan Institute for Health Security, National Institute of Infectious Diseases, Tokyo, Japan.ORCID 0000-0001-5224-2499
Yuko Okemoto-Nakamura *Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.ORCID 0009-0003-8173-7345
Hirotaka Takagi *Research Center for Biosafety, Laboratory Animal and Pathogen Bank, National Institute of Infectious Diseases, Japan Institute for Health Security, Tokyo, Japan.ORCID 0000-0002-3489-3105

Funding

Japan Agency for Medical Research and Development JP23fk0108683Japan Society for the Promotion of Science JP20K08320Japan Society for the Promotion of Science JP23K21362Japan Society for the Promotion of Science JP24K13428Ministry of Health, Labour and Welfare JPMH22KA1001Ministry of Health, Labour and Welfare JPMH25KA1001SHIONOGI INFECTIOUS DISEASE RESEARCH PROMOTION FOUNDATION
6 · The paper itself

Abstract

Human sapoviruses (HuSaVs), which cause acute gastroenteritis, are highly diverse. Fifteen HuSaV genotype strains (GI.1-7, GII.1-5, -8, and GV.1-2) were efficiently propagated in the human duodenum-derived cell line HuTu80 when supplemented with conjugated bile acid (T. Oka, T.-C. Li, K. Yonemitsu, Y. Ami, et al., J Virol 98:e00639-24, 2024, https://doi.org/10.1128/jvi.00639-24). However, the host cellular factors involved in HuSaV infection and propagation remain unidentified. Using a knockout approach, we newly identified and confirmed that CD36 is a critical cellular protein for the propagation of all 15 HuSaV genotypes tested in HuTu80 cells. When the CD36 gene was re-expressed in CD36 gene knockout HuTu80 cells, all HuSaV genotype strains, except for GI.6 and GII.3, recovered their viral propagation ability. To further demonstrate that human CD36 is critical for HuSaV propagation, we expressed human CD36 in HuSaV-insensitive non-human origin cells. Of the 15 HuSaV genotype strains tested, 10 from GI, GII, and GV (GI.3, -5, -6, GII.1-3, -5, -8, GV.1, and GV.2) were propagated in Chinese Hamster Ovary-K1 cells, and six from GII (GII.1-5, -8) were propagated in Vero cells. Although there were differences in the propagation ability between the genotypes tested, at least one of the three cell lines engineered to express the human CD36 gene acquired HuSaV propagation potential, confirming that human CD36 is an essential cellular factor for HuSaV propagation.IMPORTANCEThe host cellular factor(s) involved in the infection and propagation of sapovirus, which causes acute gastroenteritis in humans, remain unclear. By using a loss-of-gene function approach with a potential physiological infection site derived from a human cell line clone, which caused a marked cytopathic effect related to human sapovirus (HuSaV) propagation, we identified that CD36 was essential for the propagation of all 15 genotype strains of HuSaV tested. We confirmed different effects on distinct genotypes of HuSaV propagation by the re-expression of human CD36 in HuTu80 cells and human CD36 introduced into two non-human HuSaV-insensitive cells. This finding is an important step toward understanding common and genogroup/genotype-specific HuSaV propagation mechanisms, and the development of methods to control this highly contagious virus, including research on the development of anti-viral drugs and the establishment of HuSaV-susceptible animal models in the future.

Indexed as

Caliciviridae InfectionsCD36 AntigensSapovirusVirus ReplicationAnimalsCell LineCricetulusGene Knockout TechniquesGenotypeHumansCD36 AntigensCD36 protein, humanantigen ELISACD36conjugated bile acidsconventional cell linesCRISPR/Cas9 based genome-wide knockout screeninghuman sapoviruslentiviral vector

Identifiers

PMID41190813
PMCPMC12646008

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Registered trials

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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.