Evidence map›Paper›PMID 41824449›Full record

ArticleCell reports2026

De novo recovery of Ghana virus, an African bat Henipavirus, reveals differential tropism and attenuated pathogenicity compared to Nipah virus.

Griffin D Haas, Olivier Escaffre, Rebecca A Reis, Terry L Juelich, Jennifer K Smith, Lihong Zhang, Birte K Kalveram, Axel A Guzmán-Solís, Dariia Vyshenska, William Klain and 3 more

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Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

13 authors.

Griffin D HaasDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Olivier EscaffreDepartment of Pathology, University of Texas Medical Branch, Galveston, TX, USA.
Rebecca A ReisDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Terry L JuelichDepartment of Pathology, University of Texas Medical Branch, Galveston, TX, USA.
Jennifer K SmithDepartment of Pathology, University of Texas Medical Branch, Galveston, TX, USA.
Lihong ZhangDepartment of Pathology, University of Texas Medical Branch, Galveston, TX, USA.
Birte K KalveramDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Axel A Guzmán-SolísDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Dariia VyshenskaDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
William KlainDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Alexander L GreningerDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Alexander N FreibergDepartment of Pathology, University of Texas Medical Branch, Galveston, TX, USA. Electronic address: anfreibe@utmb.edu.
Benhur LeeDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: benhur.lee@mssm.edu.

Funding

Project 6 - Development of Antivirals against AlphavirusesU19AI171403 · NIAID · EMORY UNIVERSITY · PI George Robert Painter, Richard K. Plemper · 2022 to 2026
$59.7M
Development of broadly neutralizing human monoclonal antibodies against henipavirusesR01AI185102 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Benhur Lee · 2025 to 2026
$1.6M
NIAID NIH HHS R01 AI185102NIAID NIH HHS U19 AI171403
6 · The paper itself

Abstract

Henipaviruses (HNVs) like Nipah virus (NiV) and Hendra virus (HeV) represent severe zoonotic threats. Ghana virus (GhV), identified in 2012, is the only African bat henipavirus with a near-complete genome assembly. However, without isolates in culture, GhV biology, pathogenicity, and zoonotic potential remain poorly understood. Using reverse genetics, we recovered a full-length infectious clone of GhV at BSL-4 following rational reconstruction of its incomplete 3' leader and modification of a non-canonical transcriptional initiation site. GhV demonstrated restricted receptor tropism (ephrin-B2 but not ephrin-B3) and distinct innate immune antagonism. Replication was attenuated in primary human cells but was enhanced in bat cells. In Syrian golden hamsters, GhV infection caused no disease or mortality. Furthermore, a chimeric NiV encoding the GhV receptor-binding protein was completely attenuated in vivo, implicating ephrin-B3 receptor usage as a critical determinant of HNV pathogenesis. These findings elucidate GhV zoonotic potential and inform strategies for virus surveillance and control.

Indexed as

ChiropteraHenipavirusHenipavirus InfectionsNipah VirusViral TropismAnimalsCricetinaeEphrin-B2Ephrin-B3HumansMesocricetusVirulenceVirus ReplicationEphrin-B2Ephrin-B3BSL-4CP: microbiologyemerging virusesEphrin-B2Ephrin-B3Ghana virushenipavirusNipah virusreverse geneticsviral pathogenesiszoonotic potential

Identifiers

PMID41824449
PMCPMC13107972

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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.