Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this paper, we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the importance of resolution of inflammation as a way of maintaining homeostasis against oxidative stress and to prevent the ‘horror autotoxicus’ of chronic inflammation. Nevertheless, host immune regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-driven diseases, and (iii) parasitic strategies to subvert inflammation.

While the epidemic of SARS-CoV-2 has spread worldwide, there is much concern over the mortality rate that the infection induces. Available data suggest that COVID-19 case fatality rate had varied temporally (as the epidemic has progressed) and spatially (among countries). Here, we attempted to identify key factors possibly explaining the variability in case fatality rate across countries. We used data on the temporal trajectory of case fatality rate provided by the European Center for Disease Prevention and Control, and country-specific data on different metrics describing the incidence of known comorbidity factors associated with an increased risk of COVID-19 mortality at the individual level. We also compiled data on demography, economy and political regimes for each country. We found that temporal trajectories of case fatality rate greatly vary among countries. We found several factors associated with temporal changes in case fatality rate both among variables describing comorbidity risk and demographic, economic and political variables. In particular, countries with the highest values of DALYs lost to cardiovascular, cancer and chronic respiratory diseases had the highest values of COVID-19 CFR. CFR was also positively associated with the death rate due to smoking in people over 70 years. Interestingly, CFR was negatively associated with share of death due to lower respiratory infections. Among the demographic, economic and political variables, CFR was positively associated with share of the population over 70, GDP per capita, and level of democracy, while it was negatively associated with number of hospital beds ×1000. Overall, these results emphasize the role of comorbidity and socio-economic factors as possible drivers of COVID-19 case fatality rate at the population level.

Antagonistic coevolution between hosts and parasites has been proposed as a mechanism maintaining genetic diversity in both host and parasite populations. In particular, the high level of genetic diversity usually observed at the major histocompatibility complex (MHC) is generally thought to be maintained by parasite-driven selection. Among the possible ways through which parasites can maintain MHC diversity, diversifying selection has received relatively less attention. This hypothesis is based on the idea that parasites exert spatially variable selection pressures because of heterogeneity in parasite genetic structure, abundance or virulence. Variable selection pressures should select for different host allelic lineages resulting in population-specific associations between MHC alleles and risk of infection. In this study, we took advantage of a large survey of avian malaria in 13 populations of the house sparrow (Passer domesticus) to test this hypothesis. We found that (i) several MHC alleles were either associated with increased or decreased risk to be infected withPlasmodium relictum, (ii) the effects were population specific, and (iii) some alleles had antagonistic effects across populations. Overall, these results support the hypothesis that diversifying selection in space can maintain MHC variation and suggest a pattern of local adaptation where MHC alleles are selected at the local host population level.

Since the beginning of the twentieth century, infection has emerged as a fundamental aspect of cancer causation with a growing number of pathogens recognized as oncogenic. Meanwhile, oncolytic viruses have also attracted considerable interest as possible agents of tumor destruction. Lost in the dichotomy between oncogenic and oncolytic agents, the indirect influence of infectious organisms on carcinogenesis has been largely unexplored. We describe the various ways – from functional aspects to evolutionary considerations such as modernity mismatches – by which infectious organisms could interfere with oncogenic processes through immunity. Finally, we discuss how acknowledging these interactions might impact public health approaches and suggest new guidelines for therapeutic and preventive strategies both at individual and population levels. Infectious organisms, that are not oncogenic neither oncolytic, may play a significant role in carcinogenesis, suggesting the need to increase our knowledge about immune interactions between infections and cancer.

We tested the differential maternal allocation hypothesis in a population of house sparrows. We experimentally altered the attractiveness of males by treating them with implants filled with crystalline testosterone (T) or left empty (C). We subsequently monitored maternal investment as a function of male hormonal treatment and the size of the black patch of feathers on the throat (i.e., the badge), a sexually selected trait. The differential allocation hypothesis predicts that females should adjust their investment with respect to the benefits they receive by mating with an attractive male. Given that both circulating levels of T and badge size are condition-dependent traits, we expected that females mated with T males and/or with large-badged males should invest more into current reproduction. Contrary to this prediction, we found no evidence that suggested differential maternal allocation in this population of house sparrows. Female investment in yolk T, yolk mass, clutch size, chick brooding, and feeding was not affected by male hormonal treatment or by male badge size. As expected, T males invested less into chick brooding and feeding. More surprisingly, females did not compensate the reduced paternal contribution to chick feeding. As a consequence, the breeding success of T pairs was largely reduced compared with that of C pairs. The absence of differential allocation in a system in which it could have an adaptive role raises the question about the possible constraints or overriding factors operating on patterns of reproductive investment in this species.