What question did this study set out to answer?

The study aims to investigate how the host and parasite interact during infection in terms of oxidative stress responses.

January 23, 2026Open Access

Host–parasite oxidative arms race: who will win?

Puntos clave

The study aims to investigate how the host and parasite interact during infection in terms of oxidative stress responses.
Experimental infection of Eurasian siskins with Plasmodium ashfordi.
Assessment of antioxidant system responses over time.
Comparison of gene expression data from both host and parasite.
Analysis of physiological levels of glutathione.
The parasite shows high expression of antioxidant genes to combat oxidative stress.
The host upregulates protective enzymes but experiences reduced glutathione levels.
Parasitaemia decreased from 44% at day 21 to 15% at day 31, indicating the host's strategy effectively combats the parasite.

Resumen

Avian haemosporidian parasites are globally widespread with a broad repertoire of hosts. When infected, the host can either reduce (resistance) and/or limit the severity of parasitaemia (tolerance). Oxidative stress plays a pivotal role in the host's resistance and tolerance, as well as its detrimental endpoints. The rationale behind this paradox lies in the dual role of reactive oxygen species (ROS): they are both beneficial and detrimental for the host, while being harmful to the parasite. Thus, it is in the parasite's interest to maintain a reduced environment within the host's cell, whereas the host needs a fine‐tuned balance between generating ROS to eliminate the parasites and maintaining sufficient antioxidant levels to protect itself. This dynamic we refer to as the host–parasite oxidative arms race . Here, Eurasian siskins Spinus spinus were experimentally infected with Plasmodium ashfordi to investigate how the fundamental antioxidant system – the glutathione system – responds to infection over time compared to control birds. By combining physiological and gene expression data from both the parasite and the host at different time points, we provide evidence for this oxidative arms race . The gene expression data show that the parasite aims to eliminate ROS through its high expression of superoxide dismutase (SOD), glutathione reductase (GR), and glutathione synthetase. In contrast, the host upregulates glutathione S‐transferases (GSTs) and glutathione peroxidases (GPX), which may result in the reduced physiological levels of glutathione seen at the end of the experiment. Although the parasite seems to win the race in terms of the oxidative state of the cell, the marked decrease in parasitaemia from day 21 (44%) to day 31 (15%) suggests that the host's strategy is sufficient to defeat the parasite. Future studies should include measures of oxidative damage to reveal whether there are any long‐term costs related to the host's strategy at different time points of infection.

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