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Indeed, since most birds are likely to have a relapse infection, the low tGSH in old P. relictum infected birds can be a result of a more rapid decline of the antioxidant defences (or indirectly via degradation of other cellular mechanisms affecting GSH synthesis) compared to uninfected ageing birds.
Whether PVL-positive MRSA strains possess a greater potential to persistent colonization and facilitate the subsequent relapse infection needs further studies.
DOI: http://dx.doi.org/10.7554/eLife.04692.004 The within-host model can be used to simulate beyond the first relapse infection.
Time to first relapse infection from the within-host model fitted to data from three ecological zones with tropical strains of P. vivax (Battle et al., 2014 ).
The likelihood of the tropical relapse model can be evaluated by applying the model to the data on time to first relapse infection.
Figure 1 shows the best fit within-host relapse model to data on time to first relapse infection from three ecological zones with tropical strains of P. vivax: South America, South East Asia and Melanesia (Battle et al., 2014).
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However, more recently, studies using microsatellite markers identified from the Pv genome sequence showed that relapse infections often result from activation of heterologous hypnozoites [13], [14].
Control measures are confounded by two major factors: firstly, the presence of dormant hypnozoite stages in the liver, which result in relapse infections weeks after the cure of the initial episode, and secondly the emergence of chloroquine resistance.
10.7554/eLife.04692.007 Figure 3. Predicted relapse infections following primary P. vivax infection.
Patients with Plasmodium vivax malaria are treated with primaquine to prevent relapse infections.
Plasmodium vivax relapse infections occur following activation of latent liver-stages parasites (hypnozoites) causing new blood-stage infections weeks to months after the initial infection.
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