Forest soil viruses may dampen how strongly microbes respire as temperatures rise

Beneath every forest floor, an invisible war and an uneasy truce unfold simultaneously. Bacteriophages, the viruses that infect soil bacteria, can rupture their hosts in a burst of viral replication, or they can quietly integrate their genomes into bacterial chromosomes and ride along as dormant passengers, a state known as lysogeny. While viral lysis has long been appreciated as a shaper of microbial communities, the role of these lysogenic relationships in one of the planet’s most consequential carbon fluxes, the microbial respiration of forest soils, has remained largely unexplored. A new study published in Plant and Soil now links lysogenic viral processes to a striking pattern: a reduced temperature sensitivity of microbial respiration across forests spanning an enormous climatic range.

The research, led by Jia Yao and Ming Nie of Fudan University in Shanghai, together with colleagues, tackled a question with direct implications for climate modeling. Soil microbial respiration releases carbon dioxide as microbes metabolize organic matter, and the rate of that release accelerates as temperatures rise. The magnitude of this acceleration is captured by the temperature sensitivity coefficient, or Q10, which describes how much respiration increases for every ten degrees Celsius of warming. Whether Q10 varies systematically across climates, and what biological mechanisms drive that variation, remains one of the more contested issues in terrestrial carbon cycle science, with direct consequences for how strongly soils are expected to feed back into atmospheric warming.

To probe the role of lysogenic viruses, the team collected soils from 13 forest sites distributed along a 3,600-kilometer latitudinal climate gradient across China, from cool northern forests to warm subtropical ones. In the laboratory, they incubated each soil at three temperatures, 15, 25, and 35 degrees Celsius, and measured microbial respiration. Crucially, they also employed a chemical trick that has become a standard tool in viral ecology: treatment with mitomycin C, a compound that damages bacterial DNA and thereby provokes temperate prophages harbored within bacterial genomes to enter the lytic cycle. The response of a soil community to mitomycin C induction serves as an operational proxy for the abundance and activity of lysogenic viral processes in that community.

The design allowed the researchers to construct three distinct estimates of thermal sensitivity. Soils treated with mitomycin C exhibited higher Q10 values than untreated controls, indicating that chemically forcing prophages out of their lysogenic state intensified the temperature response of respiration. More intriguing was a third quantity: the Q10 calculated from the contrast between induced and uninduced soils, which the authors interpret as an SLV-associated Q10, reflecting the thermal behavior of respiration linked to lysogenic viral processes. This proxy-derived sensitivity was the lowest of the three, suggesting that processes tied to lysogenic viruses are associated with a dampened apparent response of respiration to warming.

Across the 13 sites, the variation in this SLV-associated temperature sensitivity was most strongly associated with two characteristics of the bacterial communities: their abundance and their life-history strategies. Soil bacteria are commonly sorted along a spectrum from r-strategists, which grow rapidly and opportunistically when resources are plentiful, to K-strategists, which invest in persistence, resource efficiency, and stress tolerance under more competitive conditions. Previous work has shown that the dominance of one strategy or the other shapes how microbial respiration responds to temperature, and the new findings indicate that the viral induction response is entangled with this same axis of microbial life history. Communities where lysogenic processes left a distinct imprint on respiration were also communities whose compositional and functional makeup reflected particular positions along the r-to-K spectrum.

Climate itself did not disappear from the picture, but its influence was largely indirect. The researchers used structural equation modeling, a statistical framework that allows direct and indirect pathways among variables to be separated, to trace how climatic variables propagate to the viral-linked temperature sensitivity. The analysis revealed that climate was connected to the SLV-associated Q10 through mediating factors, chiefly soil pH and the physical properties of the soil, such as texture-related characteristics. This pattern is consistent with a growing body of viral ecology showing that soil pH is a powerful determinant of viral community structure at scales from local plots to the globe. In other words, climate appears to set the stage, through the chemical and physical environment it helps create, on which lysogenic viral processes and bacterial life-history traits together govern how temperature-sensitive respiration becomes.

The geographic pattern embedded in these results is especially noteworthy. The association between the mitomycin C response and reduced apparent thermal sensitivity was strongest in warmer forest soils, implying that in the very ecosystems where microbial respiration could potentially release the most additional carbon under continued warming, lysogenic viral processes may be exerting a moderating influence. The authors are careful with their language throughout, framing the findings in terms of association rather than proof of causation. Mitomycin C induction is a blunt instrument: the compound is a DNA-damaging agent, and the observed differences between treated and untreated soils could in principle reflect the combined consequences of prophage induction, bacterial mortality, altered community composition, and the release of cellular contents. The interpretation of the induced contrast as an SLV-associated signal is therefore an operational one, a proxy rather than a direct measurement of viral behavior.

Even so, the study lands at a moment when the viral dimension of soil carbon cycling is moving rapidly from the margins to the mainstream. A global atlas of soil viruses published in 2024 catalogued an enormous and previously uncharted viral diversity and flagged potential biogeochemical impacts, while other recent work has demonstrated that viral lysis can alleviate microbial nutrient limitation and accumulate chemically recalcitrant dissolved organic matter in soils. Theoretical treatments have argued that viral infections likely mediate microbial controls on ecosystem responses to warming, but empirical tests along real climate gradients have been scarce. By combining a standardized induction assay with controlled incubations across thousands of kilometers, the new study offers one of the more systematic empirical links to date between a specific viral strategy and a keystone carbon-cycle parameter.

The mechanistic possibilities behind the observed pattern remain open. Lysogeny can benefit bacterial hosts directly: cryptic prophages can confer tolerance to environmental stress, and integrating viruses may alter host metabolism in ways that change growth rates and resource use. If lysogeny is more prevalent or more consequential in warm, low-latitude soils, and if it favors or co-occurs with K-strategist lineages whose respiration is inherently less temperature responsive, then the dampened SLV-associated Q10 would follow as an emergent property of the host-virus ecosystem. Alternatively, the induction treatment itself may reveal the scale of the lysogenic reservoir, with soils harboring more temperate phages showing different post-induction respiratory trajectories. Distinguishing among these mechanisms will require experiments that go beyond induction proxies, perhaps tracking viral and host population dynamics through time under warming.

For climate modelers, the message is both cautionary and constructive. The findings suggest that bacterial responses associated with lysogenic viral processes deserve a place in future assessments of how forest soil carbon responds to warming, particularly when evaluating microbial controls on carbon turnover. If lysogeny-associated processes genuinely reduce the thermal sensitivity of respiration in warmer forests, then current projections that ignore viral regulation may overestimate carbon losses from those systems. But because the evidence is associative and proxy-based, the authors’ conclusions point less toward immediate model revision and more toward an agenda: combining induction experiments with viromics, microbial trait measurements, and gradient sampling to pin down when, where, and how the quiet passengers in bacterial genomes bend the temperature curve of one of Earth’s largest carbon fluxes. The forest floor, it turns out, is not merely a chemical reactor warmed by the atmosphere above; it is also an arena where viruses, hosts, and climate quietly negotiate the pace of carbon’s return to the sky.

Subject of Research: Association between lysogenic soil viruses and the temperature sensitivity of forest soil microbial respiration

Article Title: Lysogenic viral processes are associated with reduced temperature sensitivity of forest soil microbial respiration

Article References: Yao, J., Xu, J., Xu, X., Liu, M., Chen, C., Bao, Y., Li, J., & Nie, M. (2026). Lysogenic viral processes are associated with reduced temperature sensitivity of forest soil microbial respiration. Plant and Soil. https://doi.org/10.1007/s11104-026-09126-x

Image Credits: AI Generated

DOI: 10.1007/s11104-026-09126-x

Keywords: lysogeny, soil viruses, bacteriophages, forest soils, microbial respiration, temperature sensitivity, Q10, carbon cycle, climate gradient, mitomycin C, bacterial life-history strategies, climate warming