The interaction between UVR and parasites

This type of interaction is obviously restricted to ectoparasites or to the free stadium of endoparasites. Although UVR is generally associated with negative effects, it may also play a positive role on species interactions. Thus, for example, the ectoparasite copepod Lepeophtheirus salmonis (salmon lice) uses photoreceptors to avoid UVR and eventually to optimise host finding (e.g., by utilizing UV contrast vision [74]).

Most of our knowledge on the interaction between UVR and parasites, however, is related to viruses, which, although considered obligatory parasites, resemble a predator-prey interaction [75]. Due to the obligatory use of the host metabolic machinery to produce new viral copies and the impossibility to repair themselves, viruses are very vulnerable to several stressors when occurring in the water column. Among other environmental factors, solar UVR affects viruses negatively by reducing their infectivity [76]. Loss of viral infectivity after exposure to solar radiation seems to be mainly caused by damage to the viral genome, although indirect damage to the capsid has also been suggested to result in inactivation [77]. Wavelengths < 320 nm are generally the most effective ones to cause viral inactivation [78], although UV-A radiation [79] and wavelengths < 556 nm [77] have been found to inactivate viruses as well. Like in many other planktonic groups, different viruses appear to have different tolerance towards solar radiation [77,78,80], but the reason(s) for this remains unclear. Kellogg and Paul [81] found that the degree of UV damage of six marine vibriophages was negatively correlated with the G -f C content and suggested that the increase of thymine dimer targets increases their sensitivity by reducing the ability to repair the damage, a hypothesis previously proposed for bacteria by Singer and Ames [82]. The DNA damage, however, can be repaired after infection takes place using the host repair mechanisms. Thus, different repair mechanisms or efficiencies may also explain the variability observed in virus inactivation rates. The infectivity of phages can be restored inside bacteria, either through a specific host-repair-machinery (= photoreactivation) [83,84] or by a virus encoded repair system [85,86]. The light-dependent repair mechanism of bacteria seems to be crucial to restore the infectivity of natural aquatic viruses [83,84,87]. Therefore, the potential recovery of viruses makes it difficult to predict the overall effect of UVR in this interaction. Moreover, the inactivation-recovery process is further complicated by the fact that the physiological status of bacteria can be also impaired by UVR [88,89],

The physical disruption/destruction of the viral particle by high-energy photons is another mechanism that can account for loss of viral abundance [90]. The exact mechanism of this destruction, however, is not well understood and the experimental results gathered with different viruses are inconclusive [91,92],

Finally, another potential interplay between UVR and viruses occurs when they coexist with their host in a type of mutualistic relationship, where the nucleic acid of the virus is integrated in the genome of the host and is replicated with it (lysogenic state). Ultraviolet C radiation produced by germicidal lamps (max. at ~ 254 nm) has normally been used, among other stressors, to induce the shift from lysogenic to lytic state in a complex mechanism involving the DNA repair SOS system of the host [93]. However, natural or simulated solar UVR seems not to be very efficient in this process [94,95].

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