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[Display omitted] • Early-life diet has been shown to affect both juvenile and adult life history traits. • Less well known are early-life diet effects on adult responses to infection. • We altered larval dietary macronutrient ratio in Drosophila melanogaster. • We then infected adult females with a bacterial pathogen Pseudomonas entomophila. • Larval diet affected adult reproduction, but not survival, even under infection. Early-life conditions have profound effects on many life-history traits, where early-life diet affects both juvenile development, and adult survival and reproduction. Early-life diet also has consequences for the ability of adults to withstand environmental challenges such as starvation, temperature and desiccation. However, it is less well known how early-life diet influences the consequences of infection in adults. Here we test whether varying the larval diet of female Drosophila melanogaster (through altering protein to carbohydrate ratio, P:C) influences the long-term consequences of injury and infection with the bacterial pathogen Pseudomonas entomophila. Given previous work manipulating adult dietary P:C, we predicted that adults from larvae raised on higher P:C diets would have increased reproduction, but shorter lifespans and an increased rate of ageing, and that the lowest larval P:C diets would be particularly detrimental for adult survival in infected individuals. For larval development, we predicted that low P:C would lead to a longer development time and lower viability. We found that early-life and lifetime egg production were highest at intermediate to high larval P:C diets, but this was independent of injury and infection. There was no effect of larval P:C on adult survival. Larval development was quickest on intermediate P:C and egg-to-pupae and egg-to-adult viability were slightly higher on higher P:C. Overall, despite larval P:C affecting several measured traits, we saw no evidence that larval P:C altered the consequence of infection or injury for adult survival or early-life and lifetime reproduction. Taken together, these data suggest that larval diets appear to have a limited impact on the adult life history consequences of infection. [ABSTRACT FROM AUTHOR]

All organisms are infected with a range of symbionts spanning the spectrum of beneficial mutualists to detrimental parasites. The fruit fly Drosophila melanogaster is a good example, as both endosymbiotic Wolbachia , and pathogenic Drosophila C Virus (DCV) commonly infect it. While the pathophysiology and immune responses against both symbionts are the focus of intense study, the behavioural effects of these infections have received less attention. Here we report sex-specific behavioural responses to these infections in D. melanogaster . DCV infection caused increased sleep in female flies, but had no detectable effect in male flies. The presence of Wolbachia did not reduce this behavioural response to viral infection. We also found evidence for a sex-specific cost of Wolbachia , as male flies infected with the endosymbiont became more lethargic when awake. We discuss these behavioural symptoms as potentially adaptive sickness behaviours. [ABSTRACT FROM AUTHOR]

Highlights: [•] Understanding the maintenance of pathogen variation is central to disease control. [•] Classical metapopulation models make useful predictions about polymorphism. [•] The timing of pathogen regulation is key to pathogen polymorphism and virulence. [Copyright &y& Elsevier]

One of the defining features of mosquito vectors of arboviruses such as Dengue and Zika is their ability to tolerate high levels of virus proliferation without suffering significant pathology. This adaptation is central to vector competence and disease spread. The molecular mechanisms, pathways, cellular and metabolic adaptations responsible for mosquito disease tolerance are still largely unknown and may represent effective ways to control mosquito populations and prevent arboviral diseases. In this review article, we describe the key link between disease tolerance and pathogen transmission, and how vector control methods may benefit by focusing efforts on dissecting the mechanisms underlying mosquito tolerance of arboviral infections. We briefly review recent work investigating tolerance mechanisms in other insects, describe the state of the art regarding the mechanisms of disease tolerance in mosquitos, and highlight the emerging role of gut microbiota in mosquito immunity and disease tolerance. • Mosquito vectors tolerate virus proliferation without significant pathology. • A balance between immune resistance and disease tolerance shapes vector competence. • The mechanisms underlying mosquito disease tolerance are underexplored. • Targeting mosquito disease tolerance may reduce arboviral transmission. [ABSTRACT FROM AUTHOR]

Disease tolerance describes an infected host's ability to maintain health independently of the ability to clear microbe loads. The Jak/Stat pathway plays a pivotal role in humoral innate immunity by detecting tissue damage and triggering cellular renewal, making it a candidate tolerance mechanism. Here, we find that in Drosophila melanogaster infected with Pseudomonas entomophila disrupting ROS -producing dual oxidase (duox) or the negative regulator of Jak/Stat Socs36E, render male flies less tolerant. Another negative regulator of Jak/Stat , G9a - which has previously been associated with variable tolerance of viral infections – did not affect the rate of mortality with increasing microbe loads compared to flies with functional G9a , suggesting it does not affect tolerance of bacterial infection as in viral infection. Our findings highlight that ROS production and Jak/Stat signalling influence the ability of flies to tolerate bacterial infection sex-specifically and may therefore contribute to sexually dimorphic infection outcomes in Drosophila. • The Jak/Stat pathway impacts disease tolerance during systemic infection with Pseudomonas entomophila. • Disrupting Duox or Socs36E render males less tolerant to systemic bacterial infection. • G9a does not affect tolerance during bacterial infection as it does during viral infection. [ABSTRACT FROM AUTHOR]