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1. Prior heat waves improve survival of field but not domesticated populations of tobacco hornworm exposed to repeated bacterial infections

   https://doi.org/10.1111/1365-2435.70001  

   Malinski, Katherine H; Willett, Christopher S; Kingsolver, Joel G (March 2025, Functional Ecology)

   Abstract In insects and other invertebrates, prior pathogen exposures can improve immune responses and survival to subsequent infections through immune priming. Alternatively, stress and metabolic costs of multiple infections can impair host immunity and survival. The effects of high‐temperature extremes on host–pathogen interactions are not well understood despite the increasing occurrence of heat waves caused by climate change.The response of insects to heat waves and pathogens depends on recent evolutionary history with selective pressures. Domestication of insect pests has occurred in lab colonies of model species, reducing selective pressures for immune and heat stress responses. Lab strains are often used in immunological or heat stress experiments to represent wild field strains, but the efficacy of this approach is seldom evaluated.Using the tobacco hornworm (Manduca sexta), we tested the impact of a heat wave during initial pathogen exposure on survival of a secondary infection withBacillus thuringiensisbacteria. We used a domesticated lab population and a naturally occurring field population ofM. sextato evaluate the impacts of recent domestication on immune and thermal responses.A heat wave during initial infection significantly increased survival of the secondaryB. thuringiensisinfection in the field, but not the lab population ofM. sexta.In the field population, survival of the repeated infection was temperature dependent: exposure to an initial infection event reduced survival of the secondary infection at the control temperature regime, consistent with a stress effect. However, a heat wave during the initial infection event increased survival of the secondary infection, consistent with immune priming effects.The results of this study demonstrate that (a) insect response to thermal stress and pathogens can depend on recent domestication and (b) responses of hosts to repeat pathogen exposures can be temperature‐dependent, suggesting that cross‐talk between the heat stress and immune memory pathways may have important consequences for host–pathogen outcomes under heat wave events. Read the freePlain Language Summaryfor this article on the Journal blog. 

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2. Immune interactions and heterogeneity in transmission drives the pathogen‐mediated invasion of grey squirrels in the UK

   https://doi.org/10.1111/1365-2656.14074  

   Howell, E; White, A; Lurz, P_W W; Boots, M (June 2024, Journal of Animal Ecology)

   Abstract Mathematical models highlighted the importance of pathogen‐mediated invasion, with the replacement of red squirrels by squirrelpox virus (SQPV) carrying grey squirrels in the UK, a well‐known example.In this study, we combine new epidemiological models, with a range of infection characteristics, with recent longitudinal field and experimental studies on the SQPV dynamics in red and grey squirrel populations to better infer the mechanistic basis of the disease interaction.A key finding is that a model with either partial immunity or waning immunity and reinfection, where individuals become seropositive on the second exposure to infection, that up to now has been shown in experimental data only, can capture the key aspects of the field study observations.By fitting to SQPV epidemic observations in isolated red squirrel populations, we can infer that SQPV transmission between red squirrels is significantly (4×) higher than the transmission between grey squirrels and as a result our model shows that disease‐mediated replacement of red squirrels by greys is considerably more rapid than replacement in the absence of SQPV.Our findings recover the key results of the previous model studies, which highlights the value of simple strategic models that are appropriate when there are limited data, but also emphasise the likely complexity of immune interactions in wildlife disease and how models can help infer disease processes from field data. 

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3. Drosophila immune priming to Enterococcus faecalis relies on immune tolerance rather than resistance

   https://doi.org/10.1371/journal.ppat.1011567  

   Cabrera, Kevin; Hoard, Duncan S.; Gibson, Olivia; Martinez, Daniel I.; Wunderlich, Zeba (August 2023, PLOS Pathogens)

   Garsin, Danielle A. (Ed.)

   Innate immune priming increases an organism’s survival of a second infection after an initial, non-lethal infection. We usedDrosophila melanogasterand an insect-derived strain ofEnterococcus faecalisto study transcriptional control of priming. In contrast to other pathogens, the enhanced survival in primed animals does not correlate with decreasedE.faecalisload. Further analysis shows that primed organisms tolerate, rather than resist infection. Using RNA-seq of immune tissues, we found many genes were upregulated in only primed flies, suggesting a distinct transcriptional program in response to initial and secondary infections. In contrast, few genes continuously express throughout the experiment or more efficiently re-activate upon reinfection. Priming experiments in immune deficient mutants revealed Imd is largely dispensable for responding to a single infection but needed to fully prime. Together, this indicates the fly’s innate immune response is plastic—differing in immune strategy, transcriptional program, and pathway use depending on infection history. 

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4. The airborne herbivore‐induced plant volatile indole is converted to benzoxazinoid defense compounds in maize plants

   https://doi.org/10.1111/nph.70004  

   Sorg, Ariel; Luo, Zhi‐Wei; Li, Qin‐Bao; Roy, Kristin; Basset, Gilles J; Kim, Jeongim; Hunter, Charles; Chapple, Clint; Rering, Caitlin; Block, Anna K (February 2025, New Phytologist)

   Summary Herbivore‐induced plant volatiles act as danger signals to prime defense responses in neighboring plants, yet in many cases the mechanism behind this priming is not known. Volatile signals may be recognized directly by receptors and/or converted into other active compounds. Here we investigate the metabolic fate of volatile indole, a known priming signal in maize (Zea mays), to determine if its conversion to other compounds could play a role in its priming of defenses.We identified benzoxazinoids as major products from volatile indole using heavy isotope‐labeled volatile indole and Pathway of Origin Determination in Untargeted Metabolomics (PODIUM) analysis. We then used benzoxazinoid biosynthesis maize mutants to investigate their role in indole‐mediated priming.Labeled volatile indole was converted into DIMBOA‐glucoside in abx2(benzoxazinone synthesis2)‐dependent manner. Thebx2mutant plants showed elevated green leaf volatile (GLV) production in response to wounding andSpodoptera frugiperdaregurgitant irrespective of indole exposure.Thus, volatile indole is converted into benzoxazinoids, and part of its priming mechanism may be due to the enhanced production of these phytoanticipins. However, indole‐mediated enhanced GLV production does not rely on the conversion of indole to benzoxazinoids, so indole also has other signaling functions. 

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5. Male pathology regardless of behaviour drives transmission in an avian host–pathogen system

   https://doi.org/10.1111/1365-2656.14026  

   Sauer, Erin L; Connelly, Chloe; Perrine, Weston; Love, Ashely C; DuRant, Sarah E (January 2024, Journal of Animal Ecology)

   Abstract Host sex is an important source of heterogeneity in the severity of epidemics. Pinpointing the mechanisms causing this heterogeneity can be difficult because differences in behaviour among sexes (e.g. greater territorial aggression in males) can bias exposure risk, obfuscating the role of immune function, which can lead to differences in pathology, in driving differential susceptibility between sexes. Thus, sex‐biased transmission driven by differences in immune function independent of behaviour is poorly understood, especially in non‐mammalian systems.Here we examine the previously unexplored potential for male‐biased pathology to affect transmission using an avian host–pathogen system. We employ a sex‐dependent multistate transmission model parameterized with isolated, individual‐based experimental exposures of domestic canaries and experimental transmission data of house finches.The experiment revealed that male birds have shorter incubation periods, longer recovery periods, higher pathogen burdens and greater disease pathology than females. Our model revealed that male‐biased pathology led to epidemic size rapidly increasing with the proportion of male birds, with a nearly 10‐fold increase in total epidemic size from an all‐female to an all‐male simulation.Our results demonstrate that female‐biased resistance, independent of male behaviour, can drive sex‐dependent transmission in wildlife, indicating that sex‐based differences in immune function, not just differences in exposure risk, can shape epidemic dynamics. 

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