GAVNet Collaborative Curation

Land use change-for example, the conversion of natural habitats to agricultural or urban ecosystems-is widely recognized to influence the risk and emergence of zoonotic disease in humans1,2. However, whether such changes in risk are underpinned by predictable ecological changes remains unclear. It has been suggested that habitat disturbance might cause predictable changes in the local diversity and taxonomic composition of potential reservoir hosts, owing to systematic, trait-mediated differences in species resilience to human pressures3,4. Here we analyse 6,801 ecological assemblages and 376 host species worldwide, controlling for research effort, and show that land use has global and systematic effects on local zoonotic host communities. Known wildlife hosts of human-shared pathogens and parasites overall comprise a greater proportion of local species richness (18-72% higher) and total abundance (21-144% higher) in sites under substantial human use (secondary, agricultural and urban ecosystems) compared with nearby undisturbed habitats. The magnitude of this effect varies taxonomically and is strongest for rodent, bat and passerine bird zoonotic host species, which may be one factor that underpins the global importance of these taxa as zoonotic reservoirs. We further show that mammal species that harbour more pathogens overall (either human-shared or non-human-shared) are more likely to occur in human-managed ecosystems, suggesting that these trends may be mediated by ecological or life-history traits that influence both host status and tolerance to human disturbance5,6. Our results suggest that global changes in the mode and the intensity of land use are creating expanding hazardous interfaces between people, livestock and wildlife reservoirs of zoonotic disease.

we really need to understand how the immune system reacts to the coronavirus.

Carbonyl sulfide (OCS) is the most stable and abundant sulfur-containing gas in the atmosphere. It is derived from both natural and anthropogenic sources and is of key interest to scientists investigating how much carbon dioxide (CO2) plants take out of the atmosphere for photosynthesis. Measuring CO2 alone cannot provide estimates of photosynthesis (taking up CO2) because plants also release CO2 through respiration. In contrast, OCS is taken up like CO2 but is not released by respiration, and can therefore provide valuable information about the rate of global photosynthesis.

Doyne Farmer - a physicist who has studied the economic impact of the COVID-19 pandemic - talks to Benjamin Skuse about lockdown easing and the prospects of financial recovery

People the world over have acquired a passing familiarity with epidemic models, critical threshold values for transmission (R0), comorbidities, and exponential growth. But these insights into the pandemic are like Harrison's H1-3; they focus on a few elements of the problem. The pandemic is every bit as much a problem of the non-linear dynamics of markets, the cognitive biases of decision-makers, the collective dynamics of groups, and the coevolution of biological species - humans, mammalian food sources, and viral agents.

BY NOW THERE'S little doubt about hydroxychloroquine: It doesn't work for treating Covid-19. But there's a bigger, more important lesson hidden in the story of its failure-a rarely-mentioned, but altogether crucial, error baked into the early research. The scientists who ran the first, promising laboratory experiments on the drug had used the wrong kind of cells: Instead of testing its effects on human lung cells, they relied on a supply of mass-produced, standardized cells made from a monkey's kidney. In the end, that poor decision made their findings more or less irrelevant to human health. Worse, it's possible that further research into novel Covid-19 cures will end up being compromised by the same mistake.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) detection platforms currently report qualitative results. However, technology based on RT-PCR allows for calculation of viral load, which is associated with transmission risk and disease severity in other viral illnesses.1 Viral load in COVID-19 might correlate with infectivity, disease phenotype, morbidity, and mortality. To date, no studies have assessed the association between viral load and mortality in a large patient cohort.2, 3, 4 To our knowledge, we are the first to report on SARS-CoV-2 viral load at diagnosis as an independent predictor of mortality in a large hospitalised cohort (n=1145).

group of researchers from three Japanese universities has discovered why the western subarctic Pacific Ocean, which accounts for only 6 percent of the world's oceans, produces an estimated 26 percent of the world's marine resources.

this is how living in the COVID era can feel. We know that an unprecedented economic cataclysm has rippled across the globe. But the precise consequences of this catastrophe - for the global economy, geopolitics, climate change, and our own little lives - remain opaque.

When telling a story, common but invisible words-a, the, it-are used in certain ways and at certain moments. In a study published in Science Advances, researchers from The University of Texas at Austin and Lancaster University in Lancaster, United Kingdom, recorded the use of such words across thousands of fictional and nonfictional stories, mapping a universal blueprint for storytelling.