Evidence map›Paper›PMID 40493685›Full record

ArticlePLoS pathogens2025

Evolutionary and structural basis of SLAMF1 utilization in morbilliviruses-Implications for host range and cross-species transmission.

Ayumu Hyodo, Fumio Seki, Kento Fukuda, Kaede Tashiro, Yuki Kitai, Yukiko Akahori, Hideko Watabe, Hiroshi Katoh, Rikuto Osaki, Daisuke Takaya and 13 more

Abstract read
In one paragraph

Article in PLoS pathogens, 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
  3. Article
  4. Article
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

23 authors.

Ayumu HyodoGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Fumio SekiDepartment of Virology 3, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan.
Kento FukudaGraduate School of System Informatics, Kobe University, Kobe, Hyogo, Japan.
Kaede TashiroGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yuki KitaiGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Yukiko AkahoriGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hideko WatabeGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Hiroshi KatohGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Rikuto OsakiGraduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
Daisuke TakayaGraduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
Norihito KawashitaSchool of Science and Engineering, Kindai University, Higashi-osaka, Osaka, Japan.
Hideo FukuharaInternational Institute for Zoonosis Control, Hokkaido University, Sapporo, Hokkaido, Japan.
Satoshi IkegameDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Tomoki YoshikawaDepartment of Virology 1, National Institute of Infectious Diseases, Musashimurayama, Tokyo, Japan.
Park EunsilDivision of Experimental Animal Research, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo, Japan.
Shigeru MorikawaDivision of Experimental Animal Research, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo, Japan.
Ryoji YamaguchiFaculty of Agriculture, University of Miyazaki, Miyazaki, Japan.
Benhur LeeDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Katsumi MaenakaFaculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Hokkaido, Japan.
Tsuyoshi ShiraiFaculty of Bioscience, Nagahama Institute of BioScience and Technology, Nagahama, Shiga, Japan.
Kaori FukuzawaGraduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
Shigenori TanakaGraduate School of System Informatics, Kobe University, Kobe, Hyogo, Japan.
Makoto TakedaGraduate School of Medicine and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.ORCID 0000-0002-8194-7727

Funding

NIAID NIH HHS R01 AI188431
6 · The paper itself

Abstract

Morbilliviruses, including measles virus (MV), canine distemper virus (CDV), peste des petits ruminants virus, and cetacean morbillivirus pose a significant threat to humans and animals. While the host range of morbilliviruses is generally well-defined, cross-species transmission events with significant mortality have also been reported. Their entry into immune cells, the primary targets of morbilliviruses, relies on the signaling lymphocytic activation molecule (SLAM), also known as SLAMF1 or CD150. In this study, we hypothesize that the ability of morbilliviruses to utilize heterologous SLAM receptors stems from evolutionarily conserved structural determinants within the SLAM protein and that minimal genetic changes in the viral receptor-binding H protein can enable adaptation to novel hosts. To test this, we systematically assessed SLAM utilization and adaptation by diverse morbilliviruses. We found that most morbilliviruses efficiently utilize SLAM from multiple host species, including Myotis bat SLAM, but not human SLAM. Only MV could efficiently utilize human SLAM. Additionally, unlike other morbilliviruses, MV utilized Myotis bat SLAM inefficiently. As an example of morbillivirus adaptation to non-host animal SLAM, we conducted an MV adaptation experiment with Myotis bat SLAM. We demonstrated that MV readily adapted to utilize Myotis bat SLAM by acquiring a single N187Y mutation in its hemagglutinin protein. Notably, hypothetical ancestral SLAMs acted as universal receptors for all morbilliviruses. These results reinforced that morbillivirus receptor usage is primarily supported by evolutionarily conserved structural features of SLAM, highlighting a molecular basis that enables morbilliviruses to rapidly adapt to diverse animal SLAMs.

Indexed as

Host SpecificityMorbillivirusMorbillivirus InfectionsSignaling Lymphocytic Activation Molecule Family Member 1AnimalsDistemper Virus, CanineDogsEvolution, MolecularHumansReceptors, VirusReceptors, VirusSignaling Lymphocytic Activation Molecule Family Member 1SLAMF1 protein, human

Identifiers

PMID40493685
PMCPMC12180634

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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.