ArticleVirologica Sinica2023
FOLR1-induced folate deficiency reduces viral replication via modulating APOBEC3 family expression.
Article in Virologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Antifolate agent aminopterin demonstrates potent anti-monkeypox virus activityMicrobiology spectrum · 2026Article
- FOLR1 Regulates the Malignant Progression of Glioblastoma through the SRC/ERK1/2 Axis.Combinatorial chemistry & high throughput screening · 2026Article
- Trends in epidemics pertaining to notifiable infectious diseases in China and prediction models for key diseases: a case study of Ziyang County.BMC public health · 2025Article
- FTO-associated osteoclastogenesis promotes alveolar bone resorption in apical periodontitis male rat via the HK1/USP14/RANK pathway.Nature communications · 2025Article
- Dolutegravir induces FOLR1 expression during brain organoid development.Frontiers in molecular neuroscience · 2024Article
- Regulatory variants of APOBEC3 genes potentially associate with COVID-19 severity in populations with African ancestry.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Folate receptor alpha (FOLR1) is vital for cells ingesting folate (FA). FA plays an indispensable role in cell proliferation and survival. However, it is not clear whether the axis of FOLR1/FA has a similar function in viral replication. In this study, we used vesicular stomatitis virus (VSV) to investigate the relationship between FOLR1-mediated FA deficiency and viral replication, as well as the underlying mechanisms. We discovered that FOLR1 upregulation led to the deficiency of FA in HeLa cells and mice. Meanwhile, VSV replication was notably suppressed by FOLR1 overexpression, and this antiviral activity was related to FA deficiency. Mechanistically, FA deficiency mainly upregulated apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B) expression, which suppressed VSV replication in vitro and in vivo. In addition, methotrexate (MTX), an FA metabolism inhibitor, effectively inhibited VSV replication by enhancing the expression of APOBEC3B in vitro and in vivo. Overall, our present study provided a new perspective for the role of FA metabolism in viral infections and highlights the potential of MTX as a broad-spectrum antiviral agent against RNA viruses.
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