Predator or provider? How wild animals respond to mixed messages from humans.

Wild animals encounter humans on a regular basis, but humans vary widely in their behaviour: whereas many people ignore wild animals, some people present a threat, while others encourage animals' presence through feeding. Humans thus send mixed messages to which animals must respond appropriately to be successful. Some species appear to circumvent this problem by discriminating among and/or socially learning about humans, but it is not clear whether such learning strategies are actually beneficial in most cases. Using an individual-based model, we consider how learning rate, individual recognition (IR) of humans, and social learning (SL) affect wild animals' ability to reach an optimal avoidance strategy when foraging in areas frequented by humans. We show that 'true' IR of humans could be costly. We also find that a fast learning rate, while useful when human populations are homogeneous or highly dangerous, can cause unwarranted avoidance in other scenarios if animals generalize. SL reduces this problem by allowing conspecifics to observe benign interactions with humans. SL and a fast learning rate also improve the viability of IR. These results provide an insight into how wild animals may be affected by, and how they may cope with, contrasting human behaviour.

Rapid Assessment of SARS-CoV-2 Transmission Risk for Fecally Contaminated River Water.

Following the outbreak of severe acute respiratory syndrome coronavirus (SARS-CoV-2), airborne water droplets have been identified as the main transmission route. Identifying and breaking all viable transmission routes are critical to stop future outbreaks, and the potential of transmission by water has been highlighted. By modifying established approaches, we provide a method for the rapid assessment of the risk of transmission posed by fecally contaminated river water and give example results for 39 countries. The country relative risk of transmission posed by fecally contaminated river water is related to the environment and the populations' infection rate and water usage. On the basis of in vitro data and using temperature as the primary controller of survival, we then demonstrate how viral loads likely decrease after a spill. These methods using readily available data suggest that sewage spills into rivers within countries with high infection rates could provide infectious doses of >40 copies per 100 mL of water. The approach, implemented in the supplementary spreadsheet, can provide a fast estimate of the upper and lower viral load ranges following a riverine spill. The results enable evidence-based research recommendations for wastewater epidemiology and could be used to evaluate the significance of fecal-oral transmission within freshwater systems.

Revised estimates of ocean-atmosphere CO2 flux are consistent with ocean carbon inventory.

The ocean is a sink for ~25% of the atmospheric CO2 emitted by human activities, an amount in excess of 2 petagrams of carbon per year (PgC yr-1). Time-resolved estimates of global ocean-atmosphere CO2 flux provide an important constraint on the global carbon budget. However, previous estimates of this flux, derived from surface ocean CO2 concentrations, have not corrected the data for temperature gradients between the surface and sampling at a few meters depth, or for the effect of the cool ocean surface skin. Here we calculate a time history of ocean-atmosphere CO2 fluxes from 1992 to 2018, corrected for these effects. These increase the calculated net flux into the oceans by 0.8-0.9 PgC yr-1, at times doubling uncorrected values. We estimate uncertainties using multiple interpolation methods, finding convergent results for fluxes globally after 2000, or over the Northern Hemisphere throughout the period. Our corrections reconcile surface uptake with independent estimates of the increase in ocean CO2 inventory, and suggest most ocean models underestimate uptake.

Multiscale Immune Selection and the Transmission-Diversity Feedback in Antigenically Diverse Pathogen Systems.

Antigenic diversity is commonly used by pathogens to enhance their transmission success. Within-host clonal antigenic variation helps to maintain long infectious periods, whereas high levels of allelic diversity at the population level significantly expand the pool of susceptible individuals. Diversity, however, is not necessarily a static property of a pathogen population but in many cases is generated by the very act of infection and transmission, and it is therefore expected to respond dynamically to changes in transmission and immune selection. We hypothesized that this coupling creates a positive feedback whereby infection and disease transmission promote the generation of diversity, which itself facilitates immune evasion and further infections. To investigate this link in more detail, we considered the human malaria parasite Plasmodium falciparum, one of the most important antigenically diverse pathogens. We developed an individual-based model in which antigenic diversity emerges as a dynamic property from the underlying transmission processes. Our results show that the balance between stochastic extinction and the generation of new antigenic variants is intrinsically linked to within-host and between-host immune selection. This in turn determines the level of diversity that can be maintained in a given population. Furthermore, the transmission-diversity feedback can lead to temporal lags in the response to natural or intervention-induced perturbations in transmission rates. Our results therefore have important implications for monitoring and assessing the effectiveness of disease control efforts.

Maintenance of phenotypic diversity within a set of virulence encoding genes of the malaria parasite Plasmodium falciparum.

Infection by the human malaria parasite Plasmodium falciparum results in a broad spectrum of clinical outcomes, ranging from severe and potentially life-threatening malaria to asymptomatic carriage. In a process of naturally acquired immunity, individuals living in malaria-endemic regions build up a level of clinical protection, which attenuates infection severity in an exposure-dependent manner. Underlying this shift in the immunoepidemiology as well as the observed range in malaria pathogenesis is the var multigene family and the phenotypic diversity embedded within. The var gene-encoded surface proteins Plasmodium falciparum erythrocyte membrane protein 1 mediate variant-specific binding of infected red blood cells to a diverse set of host receptors that has been linked to specific disease manifestations, including cerebral and pregnancy-associated malaria. Here, we show that cross-reactive immune responses, which minimize the within-host benefit of each additionally expressed gene during infection, can cause selection for maximum phenotypic diversity at the genome level. We further show that differential functional constraints on protein diversification stably maintain uneven ratios between phenotypic groups, in line with empirical observation. Our results thus suggest that the maintenance of phenotypic diversity within P. falciparum is driven by an evolutionary trade-off that optimizes between within-host parasite fitness and between-host selection pressure.