Influence of delayed density and ultraviolet radiation on caterpillar granulovirus infection and mortality

1. Infectious disease is an important potential driver of population cycles, but this must occur through delayed density-dependent infection and resulting fitness effects. Delayed density-dependent infection by baculoviruses can be caused by environmental persistence of viral occlusion bodies, which can be influenced by environmental factors. In particular, ultraviolet radiation is potentially important in reducing the environmental persistence of viruses by inactivating viral occlusion bodies. 2. Delayed density-dependent viral infection has rarely been observed empirically at the population level although theory predicts that it is necessary for these pathogens to drive population cycles. Similarly, field studies have not examined the potential effects of ultraviolet radiation on viral infection rates in natural animal populations. We tested if viral infection is delayed density-dependent with the potential to drive cyclic dynamics and if ultraviolet radiation influences viral infection. 3. We censused 18 moth populations across nearly 9° of latitude over two years and quantified the effects of direct and delayed density and ultraviolet radiation on granulovirus infection rate, infection severity, and survival to adulthood. Caterpillars were collected from each population in the field and reared in the laboratory. 4. We found that infection rate, infection severity, and survival to adulthood exhibited delayed density-dependence. Ultraviolet radiation in the previous summer decreased infection severity, and increased survival probability of the virus. Structural equation modelling found that the effect of lagged density on moth survival was mediated through infection rate and infection severity, and was 2.5 fold stronger than the effect of ultraviolet radiation on survival through infection severity. 5. Our findings provide clear evidence that delayed density dependence can arise through viral infection rate and severity in insects, which supports the role of viral disease as a potential mechanism, among others, that may drive insect population cycles. Furthermore, our findings support predictions that ultraviolet radiation can modify viral disease dynamics in insect populations, most likely through attenuating viral persistence in the environment. ### Competing Interest Statement The authors have declared no competing interest.