Shortcomings of reusing species interaction networks created by different sets of researchers.

Given the requisite cost associated with observing species interactions, ecologists often reuse species interaction networks created by different sets of researchers to test their hypotheses regarding how ecological processes drive network topology. Yet, topological properties identified across these networks may not be sufficiently attributable to ecological processes alone as often assumed. Instead, much of the totality of topological differences between networks-topological heterogeneity-could be due to variations in research designs and approaches that different researchers use to create each species interaction network. To evaluate the degree to which this topological heterogeneity is present in available ecological networks, we first compared the amount of topological heterogeneity across 723 species interaction networks created by different sets of researchers with the amount quantified from non-ecological networks known to be constructed following more consistent approaches. Then, to further test whether the topological heterogeneity was due to differences in study designs, and not only to inherent variation within ecological networks, we compared the amount of topological heterogeneity between species interaction networks created by the same sets of researchers (i.e., networks from the same publication) with the amount quantified between networks that were each from a unique publication source. We found that species interaction networks are highly topologically heterogeneous: while species interaction networks from the same publication are much more topologically similar to each other than interaction networks that are from a unique publication, they still show at least twice as much heterogeneity as any category of non-ecological networks that we tested. Altogether, our findings suggest that extra care is necessary to effectively analyze species interaction networks created by different researchers, perhaps by controlling for the publication source of each network.

Testing Whether Higher Contact Among the Vaccinated Can Be a Mechanism for Observed Negative Vaccine Effectiveness.

Evidence from early observational studies suggested negative vaccine effectiveness (${V}_{Eff}$) for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) Omicron variant. Since true ${V}_{Eff}$ is unlikely to be negative, we explored how differences in contact among vaccinated persons (e.g., potentially from the implementation of vaccine mandates) could lead to observed negative ${V}_{Eff}$. Using a susceptible-exposed-infectious-recovered (SEIR) transmission model, we examined how vaccinated-contact heterogeneity, defined as an increase in the contact rate only between vaccinated individuals, interacted with 2 mechanisms of vaccine efficacy: vaccine efficacy against susceptibility ($V{E}_S$) and vaccine efficacy against infectiousness ($V{E}_I$), to produce underestimated and in some cases, negative measurements of ${V}_{Eff}$. We found that vaccinated-contact heterogeneity led to negative estimates when $V{E}_I$, and especially $V{E}_S$, were low. Moreover, we determined that when contact heterogeneity was very high, ${V}_{Eff}$ could still be underestimated given relatively high vaccine efficacies (0.7), although its effect on ${V}_{Eff}$ was strongly reduced. We also found that this contact heterogeneity mechanism generated a signature temporal pattern: The largest underestimates and negative measurements of ${V}_{Eff}$ occurred during epidemic growth. Overall, our research illustrates how vaccinated-contact heterogeneity could have feasibly produced negative measurements during the Omicron period and highlights its general ability to bias observational studies of ${V}_{Eff}$.

Observed negative vaccine effectiveness could be the canary in the coal mine for biases in observational COVID-19 studies.

Since the emergence of the SARS-CoV-2 Omicron variant, multiple observational studies have reported negative vaccine effectiveness (VE) against infection, symptomatic infection, and even severity (hospitalization), potentially leading to an interpretation that vaccines were facilitating infection and disease. However, current observations of negative VE likely stem from the presence of various biases (e.g., exposure differences, testing differences). Although negative VE is more likely to arise when true biological efficacy is generally low and biases are large, positive VE measurements can also be subject to the same mechanisms of bias. In this perspective, we first outline the different mechanisms of bias that could lead to false-negative VE measurements and then discuss their ability to potentially influence other protection measurements. We conclude by discussing the use of suspected false-negative VE measurements as a signal to interrogate the estimates (quantitative bias analysis) and to discuss potential biases when communicating real-world immunity research.

Effect of the incremental protection of previous infection against Omicron infection among individuals with a hybrid of infection- and vaccine-induced immunity: a population-based cohort study in Canada.

OBJECTIVES: We examined the incremental protection and durability of infection-acquired immunity against Omicron infection in individuals with hybrid immunity in Ontario, Canada. METHODS: We followed up 6 million individuals with at least one multiplex reverse transcriptase-polymerase chain reaction test before November 21, 2021, until an Omicron infection. Protection via infection-acquired immunity was assessed by comparing Omicron infection risk between previously infected individuals and those without documented infection under different vaccination scenarios and stratified by time since the last infection or vaccination. RESULTS: A previous infection was associated with 68% (95% CI 61-73) and 43% (95% CI 27-56) increased protection against Omicron infection in individuals with two and three doses, respectively. Among individuals with two-dose vaccination, the incremental protection of infection-induced immunity decreased from 79% (95% CI 75-81) within 3 months after vaccination or infection to 27% (95% CI 14-37) at 9-11 months. In individuals with three-dose vaccination, it decreased from 57% (95% CI 50-63) within 3 months to 37% (95% CI 19-51) at 3-5 months after vaccination or infection. CONCLUSION: Previous SARS-CovV-2 infections provide added cross-variant immunity to vaccination. Given the limited durability of infection-acquired protection in individuals with hybrid immunity, its influence on shield-effects at the population level and reinfection risks at the individual level may be limited.

How network size strongly determines trophic specialisation: A technical comment on Luna et al. (2022).

Luna et al. (2022) concluded that the environment contributes to explaining specialisation in open plant-pollinator networks. When reproducing their study, we instead found that network size alone largely explained the variation in their specialisation metrics. Thus, we question whether empirical network specialisation is driven by the environment.

The stress of Arctic warming on polar bears.

Arctic ecosystems are changing rapidly in response to climate warming. While Arctic mammals are highly evolved to these extreme environments, particularly with respect to their stress axis, some species may have limited capacity to adapt to this change. We examined changes in key components of the stress axis (cortisol and its carrier protein-corticosteroid binding globulin [CBG]) in polar bears (Ursus maritimus) from western Hudson Bay (N = 300) over a 33 year period (1983-2015) during which time the ice-free period was increasing. Changing sea ice phenology limits spring hunting opportunities and extends the period of onshore fasting. We assessed the response of polar bears to a standardized stressor (helicopter pursuit, darting, and immobilization) during their onshore fasting period (late summer-autumn) and quantified the serum levels of the maximum corticosteroid binding capacity (MCBC) of CBG, the serum protein that binds cortisol strongly, and free cortisol (FC). We quantified bear condition (age, sex, female with cubs or not, fat condition), sea ice (breakup in spring-summer, 1 year lagged freeze-up in autumn), and duration of fasting until sample collection as well as cumulative impacts of the latter environmental traits from the previous year. Data were separated into "good" years (1983-1990) when conditions were thought to be optimal and "poor" years (1991-2015) when sea ice conditions deteriorated and fasting on land was extended. MCBC explained 39.4% of the variation in the good years, but only 28.1% in the poor ones, using both biological and environmental variables. MCBC levels decreased with age. Changes in FC were complex, but more poorly explained. Counterintuitively, MCBC levels increased with increased time onshore, 1 year lag effects, and in poor ice years. We conclude that MCBC is a biomarker of stress in polar bears and that the changes we document are a consequence of climate warming.