---
title: "Single-cell organoid study links PHGDH to West Nile virus neural tropism and antiviral targeting"
id: "biorxiv-1-single-cell-analysis-of-west-nile-virus-infection-in-brain-organoids-identified"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-1-single-cell-analysis-of-west-nile-virus-infection-in-brain-organoids-identified"
content_type: "clinical_feed_article"
specialty: "Neurology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1?rss=1"
published_at: "2026-10-24T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Single-cell organoid study links PHGDH to West Nile virus neural tropism and antiviral targeting
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-1-single-cell-analysis-of-west-nile-virus-infection-in-brain-organoids-identified
- **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1?rss=1)
- **Published At:** 2026-10-24T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators built a reproducible human cerebral organoid model to study **West Nile virus** (WNV) infection in human neural tissue using virus-inclusive single-cell RNA sequencing (scRNA-Seq). - The cohort showed preferential viral tropism for neural progenitor cells, immature neurons, and astrocytes; mature neurons were largely resistant to infection. - Data indicated astrocytes were the principal source of **interferon** and acted as the main hub for IFN signalling across infected organoids, while mature neurons expressed little viral RNA-sensing machinery and low STAT1. - Differential expression analysis between permissive and nonpermissive cells revealed high baseline expression of serine synthesis and one-carbon metabolism genes (PHGDH, SHMT2, MTHFD2) in virus-susceptible cells; these genes were not induced by infection. - The study team used RNA interference and pharmacological inhibition targeting **PHGDH**; both approaches restricted WNV replication, supporting a functional requirement for this enzyme in viral replication within the organoid model. - Authors reported that the serine synthesis pathway genes mark cellular susceptibility and represent a potentially druggable antiviral target, based on the observed replication restriction after PHGDH perturbation. - The preprint status was noted; the abstract and main text are from a bioRxiv preprint and have not undergone peer review. The source did not provide full methodological details in the abstract about dosing, inhibitor identity, or precise experimental parameters. - Remaining questions recorded by the authors include validation in vivo, long-term effects of pathway inhibition on neural viability, and translation to clinical antiviral strategies; those points were mentioned in the source but without specific next-step experiments or timelines.
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Michael Leitner 1 QIMR Berghofer Medical Research Institute; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Michael%2BLeitner%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Leitner%20M&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMichael%2BLeitner%2B) * [ORCID record for Michael Leitner](http://orcid.org/0000-0003-2332-6305 "Open in new tab") Lachlan De Hayr 2 University of Queensland * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Lachlan%2BDe%2BHayr%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=De%20Hayr%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALachlan%2BDe%2BHayr%2B) * [ORCID record for Lachlan De Hayr](http://orcid.org/0000-0001-7852-2800 "Open in new tab") Ziyao Zhao 1 QIMR Berghofer Medical Research Institute; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Andrii%2BSlonchak%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Slonchak%20A&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAndrii%2BSlonchak%2B) * [ORCID record for Andrii Slonchak](http://orcid.org/0000-0003-3258-0508 "Open in new tab") * For correspondence: andrii.slonchak@qimrb.edu.au * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5901178/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5901178/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5901178/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5901178/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.23.761475v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5901178/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract The cellular and molecular determinants of human neuroinvasive West Nile virus (WNV) disease are currently poorly defined. Previous studies of WNV neural infection relied on rodent models and immortalised cell lines that diverge from human brain tissue. Herein, we established a reproducible human cerebral organoid model of WNV infection and profiled it by virus-inclusive single-cell RNA sequencing (scRNA-Seq) to obtain an understanding of WNV-host interactions in the context of human neural tissue. We found that WNV showed preferential tropism to progenitor cells, immature neurons, and astrocytes, while the mature neurons were largely resistant to infection. Astrocytes were identified as the principal source of interferon (IFN) and the main hub of IFN-signalling, whereas mature neurons expressed little viral RNA-sensing machinery or STAT1 and responded weakly to infection and to IFN. The differential gene expression analysis between WNV-permissive and nonpermissive cells demonstrated that virus-susceptible cells had high baseline expression of the serine synthesis and one-carbon metabolism genes PHGDH, SHMT2, and MTHFD2, which were not induced by infection. RNA-interference and pharmacological inhibition of phosphoglycerate dehydrogenase (PHGDH) restricted WNV replication, confirming the requirement of this gene for WNV
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