Conclusions
Little is known about the ecology of APV in natural aphid populations. But given the infection costs identified here and elsewhere, along with the rapid spread of this virus through multiple mechanisms, outbreaks may occur which significantly alter aphid population dynamics with effects that reverberate through the food web (Laubscher and Von Wechmar 1993, Ban et al. 2008, Jiang et al. 2014, Gupta et al. 2017, Dupont et al. 2020). Absent other factors, APV outbreaks would likely select for aphids carrying R. insecticola , and against those with H. defensa , which would reduce the populations’ potential to respond to subsequent increases in parasitism pressure, while enhancing protection against fungal pathogens. Alternatively, high parasitism rates, which select for H. defensa (Oliver et al. 2008, Smith et al. 2015, Hrček et al. 2016, Ives et al. 2020) potentially limit this aphid’s capacity to respond to APV outbreaks. Finally, of practical concern, we note from recent experience that APV infections spread readily in pea aphids held under common laboratory conditions. While APV infections did not influence symbiont-mediated protective phenotypes, they did impact fitness measures in the absence of enemy challenge and hence have the potential to impact a range of lab-based studies. We note that the low rates of vertical transmission, combined with PCR-based screening, allow for the ready elimination of APV from valuable experimental lines without the need to discard them.