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Its reproduction significantly retards host growth and decreases cell viability without causing lysis.
We showed that the correct characterization of the disease-free host growth is crucial for defining optimal disease control strategies.
However, these pathways rarely function optimally when first introduced into the host organism and can often deleteriously affect host growth, resulting in suboptimal yields of the desired product.
The common name of the plant reflects the dramatic effect it has on affected crops, seeming to magically arrest host growth and devastate yields.
Pseudolysogeny occurs when a host cell encounters unfavourable growth conditions and appears to play an important role in phage survival by enabling the preservation of the phage genome until host growth conditions have become advantageous again.
Host growth is shown to be important not only in controlling the supply of susceptible tissue but more subtlely in speeding up or slowing down epidemics as plants respond to disease.
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For example, a fitness cost that impairs within-host growth rates may also lengthen the duration of resistant infections, or change the transmission probabilities.
It is however possible, for the fitness cost of resistance to occur in one or in several other stages of the parasites' life cycle, resulting for example in impaired within-host growth, or lower transmission probabilities.
Traits facilitating establishment of infection can impair subsequent within-host growth (Sacristan and Garcia-Arenal 2008; Bahri et al. 2009), and in turn, within-host growth rate can impact timing and quantity of reproductive output (spore production).
Indeed, we found that parasite within-host growth rates were higher in well-fed hosts (figure 2).
Hence in this model, coinfection does not lead to selection to increase in the within-host growth rate.
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