# Synergistic Effects of Viruses and Environmental Gradients on Carbon Cycling in a River Ecosystem

**Authors:** Rongxu Luo, Hanchen Deng, Senjie Lin, Jun Bo, Weijing Kong, Shuhang Wang, Shuping Wang

PMC · DOI: 10.3390/biology15040327 · Biology · 2026-02-13

## TL;DR

This study shows how viruses in rivers influence carbon cycling, especially in agricultural areas, by responding to land use and nitrogen levels.

## Contribution

The study reveals viruses as key environmental signal transducers in river carbon cycling, integrating viral ecology into biogeochemical models.

## Key findings

- Viral activity peaks in agricultural plains, redirecting host carbon metabolism.
- Cropland coverage increases TCA cycle transcription by 1.8-fold via viral gene expression.
- Nitrogen loading suppresses both viral activity and carbon fixation in river ecosystems.

## Abstract

Rivers play a pivotal yet underexplored role in the global carbon cycle, particularly regarding viral regulation of eukaryotic carbon processing across landscapes. Through meta-transcriptomic profiling along the Yongding River, we uncovered significant spatial disparities, with viral genes—notably those encoding major capsid proteins of large DNA viruses—and eukaryotic genes involved in carbon fixation, conversion, and metabolism exhibiting peak activity in agricultural plains. Integrated analyses revealed that land use intensifies viral activity, which subsequently redirects host carbon metabolism. Structural equation modeling demonstrated that cropland coverage elevates viral expression, correlating with a 1.8-fold increase in TCA cycle transcription, while nitrogen loading suppresses both viral activity and carbon fixation. Phylogenetic evidence supports virus–host specificity as a mechanistic driver. These findings position viruses as critical environmental signal transducers that shape riverine carbon cycling, underscoring the necessity of incorporating viral ecology into predictive biogeochemical models under global change.

Riverine ecosystems represent critical nodes in the global carbon cycle, where the mechanistic role of viruses in modulating eukaryotic carbon cycling remains underexplored, particularly across heterogeneous landscapes. Here, we applied metatranscriptomics to dissect how multi-scale environmental factors and viral gene activity jointly regulate the spatial transcription of carbon cycling genes in riverine eukaryotic communities along the Yongding River, China. Our analyses reveal pronounced spatial heterogeneity in both viral gene expression—notably major capsid proteins of large eukaryotic DNA viruses—and carbon fixation, conversion, and metabolism pathways, peaking in agriculturally impacted plain regions. Multivariate statistics and network analyses demonstrate that land use enhances viral gene activity, serving as biological amplifiers that modulate host carbon metabolism and transformation. Structural equation modeling further identifies a cascade in which cropland coverage elevates viral gene expression, ultimately driving a 1.8-fold increase in TCA cycle gene transcription in plain regions, whereas nitrogen loading at the site scale suppresses viral activity and carbon fixation. Phylogenetic analysis corroborates that virus–host specificity underpins these spatial patterns. Collectively, these findings advance a new model in which viruses act as key intermediaries, transmitting multiscale environmental signals to shape riverine carbon cycling. Our study highlights the urgency of incorporating viral ecology into predictive frameworks of riverine biogeochemical cycling under accelerating environmental change.

## Linked entities

- **Chemicals:** nitrogen (PubChem CID 947)

## Full-text entities

- **Genes:** CXCL11 (C-X-C motif chemokine ligand 11) [NCBI Gene 6373] {aka H174, I-TAC, IP-9, IP9, SCYB11, SCYB9B}, ME2 (malic enzyme 2) [NCBI Gene 4200] {aka ODS1}, DNAH8 (dynein axonemal heavy chain 8) [NCBI Gene 1769] {aka ATPase, SPGF46, hdhc9}, GOLPH3 (golgi phosphoprotein 3) [NCBI Gene 64083] {aka GOPP1, GPP34, MIDAS, Vps74}, CD46 (CD46 molecule) [NCBI Gene 4179] {aka AHUS2, MCP, MIC10, TLX, TRA2.10}, DDX46 (DEAD-box helicase 46) [NCBI Gene 9879] {aka PRPF5, Prp5}, GLDC (glycine decarboxylase) [NCBI Gene 2731] {aka GCE, GCE1, GCSP, HYGN1}, PEPC (peptidase C) [NCBI Gene 5183], HFM1 (helicase for meiosis 1) [NCBI Gene 164045] {aka MER3, POF9, SEC63D1, Si-11, Si-11-6, helicase}
- **Diseases:** infection (MESH:D007239), injury to (MESH:D014947)
- **Chemicals:** Cr (MESH:D002857), Se (MESH:D012643), carbohydrate (MESH:D002241), TCA (MESH:D014238), Carbon Fate (-), Cd (MESH:D002104), As (MESH:D001151), Pb (MESH:D007854), heavy metal (MESH:D019216), citrate (MESH:D019343), CO2 (MESH:D002245), lignin (MESH:D008031), N (MESH:D009584), Carbon (MESH:D002244), carbonate (MESH:D002254), DOC (MESH:D000090422), Zn (MESH:D015032), oxygen (MESH:D010100), P (MESH:D010758), DEPC (MESH:D004047), Cu (MESH:D003300), Water (MESH:D014867)
- **Species:** Homo sapiens (human, species) [taxon 9606], Viruses (acellular root) [taxon 10239], PX clade (clade) [taxon 569578]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12937692/full.md

## References

41 references — full list in the complete paper: https://tomesphere.com/paper/PMC12937692/full.md

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Source: https://tomesphere.com/paper/PMC12937692