Wildlife trade increases pathogen transmission: What 40 years of data say about spillover
Analysis of 40 years of wildlife trade data shows that traded wild mammals are 1.5 times more likely to share pathogens with humans than non-traded species, with risk increasing for illegally or live-traded animals. Each decade a species is present in trade adds, on average, one additional shared pathogen. These findings underscore the need for enhanced biosurveillance and reduced wildlife trade to limit zoonotic disease emergence.
Hedgehogs, elephants, pangolins, bears or fennec foxes: many wild species are sold as pets, hunting trophies, for traditional medicine, biomedical research, or for their meat or fur. These practices, whether legal or illegal, concern one-quarter of all mammal species. Now a study quantifies the impact of wildlife trade on the exchange of germs and parasites between animals and humans. The work, titled "Wildlife trade drives animal-to-human pathogen transmission over 40 years," appears in Science.
The team combined forty years of legal and illegal wildlife import-export data with compilations of host–pathogen relationships. Their analyses, led to the following result: Wild mammals that are traded are 1.5 times more likely to share infectious agents with humans than those that are not involved in trade.

In other words, these species have a 50% higher probability of sharing at least one virus, bacterium, fungus or parasite with us. That is not all: the risk is even higher when species are traded illegally or alive (for example as exotic pets).
The most striking finding, according to the research team, is that "the length of time an animal has been present in trade plays a key role: On average, a species shares one additional pathogen with humans for every ten-year period spent on the market.
The results of the study highlight the need to improve biosurveillance of animals and animal-derived products in order to detect infectious agents and assess their potential for transmission to humans.

Jérôme M. W. Gippet, Wildlife trade drives animal-to-human pathogen transmission over 40 years, Science (2026). DOI: 10.1126/science.adw5518. www.science.org/doi/10.1126/science.adw5518

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017