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.