Since its first release in 2013, the sequence read trimming tool AlienTrimmer has been continuously improved, for use in various practical cases. In this context, the growing popularity of nanopore sequencing has made it necessary to update AlienTrimmer to deal with such long reads. New features were then implemented while guaranteeing that AlienTrimmer can still run fast. As illustrated in this note, the last release of AlienTrimmer can now filter out troublesome bases (i.e., low-quality and/or exogenous bases) from nanopore read ends with both first-rate accuracy and speed. Availability: the source code of AlienTrimmer is available at https://gitlab.pasteur.fr/GIPhy/AlienTrimmer
Prof. Amos Bairoch (1957–2025) was one of the most influential and transformative figures in modern bioinformatics, a scientist whose vision reshaped how biological information is curated, accessed, and understood. As the creator of Swiss-Prot, UniProtKB/Swiss-Prot, PROSITE, ENZYME, and several other foundational databases, he defined the gold standard for accuracy, manual curation, and open accessibility in protein knowledgebases. His work enabled generations of researchers and laid the groundwork for breakthroughs across genomics, proteomics, biotechnology, precision medicine, and systems biology.A professor at the University of Geneva and a driving force at the Swiss Institute of Bioinformatics (SIB), Prof. Bairoch dedicated his life to building high-quality, sustainable, community-oriented resources that serve millions of users worldwide. He was not only an exceptional innovator but also a generous mentor and a passionate advocate for open science, training and inspiring countless scientists who continue to carry forward his vision.The EMBnet community mourns his sudden passing with profound sadness. Amos was a colleague, collaborator, and friend whose impact on our field—and on global Life Sciences—cannot be overstated. His legacy endures in the resources he created, the standards he established, and the many people whose careers he touched. We honour his memory with deep respect, gratitude, and heartfelt sorrow.
This article addresses the genetic and genomic determinants that influence susceptibility or resistance to human infections, whether caused by bacteria, viruses, fungi, parasites or even prions. A large number of genes are involved in susceptibility or resistance, and this is because Homo sapiens sapiens evolutionarily acquired key DNA modifications adaptable to defence as a result of the interaction of infectious agents with their genetic properties, natural selection and mutations. This article provides a description of the methods used in the investigation of this evolution and mutual host-infectious agent adaptation. The genes involved in susceptibility and resistance are presented, as well as the polymorphic variants that provide greater or lesser reaction capacity. The high number of genes, which produce specific defence proteins, have intricate relationships among them. Relationships among these genes have been analysed. A list of variants, and even mutations of the 70 to 153 proteins/genes that are involved in the immune response to infectious diseases has been compiled. Additionally, we designed a network of physical interactions as predictable, with BioGrid data and enrichment data obtained by the g:Profiler platform, finding 57 of the 70 genes with protein-to-protein interactions. The network detected is composed of 1,049 interacting genes (in total 1,106 genes and 1,910 interactions). This analysis shows the importance of immunity genes in the defence against infectious agents, as well as the effects of the genes involved such as HLA, immunoglobulins, interleukins, immune cells, among others. Based on the functional analysis of genes involved in susceptibility and resistance to infections, we compiled a list of genetic disorders that increase an individual’s risk of developing infectious diseases. It is known that infectious diseases manifest general clinical characteristics, which are a good guide to suspect a disease. Furthermore, we describe general clinical signs that may suggest underlying genetic immunodeficiency and highlight specific infectious diseases—such as HIV/AIDS, amebiasis, malaria, Chagas disease, tuberculosis, and COVID-19—where genetic susceptibility factors have been well-characterised.
The spread of pathogens by animals is a serious issue around the world that causes a severe threat to human health. Feral pigeons (Columba livia forma domestica) that live in urban areas are zoonotic carriers of various pathogens that can be transmitted to humans by faecal contamination. This study aimed to detect the presence of bacterial, viral, and specifically fungal pathogens in pigeon faeces based on the World Health Organization's (WHO) priority pathogen list published in 2022. Fresh faecal samples were collected at Uppsala, Central Station, and Svandammen, the pigeons' most relevant gathering spots and feeding sites. Genomic DNA was directly extracted from these samples, and ScilifeLab performed High throughput sequencing through Oxford Nanopore Technologies(ONT) (PromethION). Metagenomic analysis revealed that most of the critically prioritized viral and bacterial pathogens listed by WHO were present in pigeon faeces. Regarding fungal pathogens, which were the main objective of this study, samples from both studied locations contained all critical, high and, medium-important fungal pathogens published in the WHO list, such as Aspergillus fumigatus, Candida albicans, Candida auris, Cryptococcus neoformans, Nakaseomyces glabratus, Candida tropicalis, and Cryptococcus gattii. These fungal pathogens pose the risk of invasive fungal diseases and severe infections in low-immunity individuals and vulnerable populations. The findings indicate the importance of conducting further research to comprehensively understand potential exposure to feral pigeons. Furthermore, keeping pigeons away from sensitive areas, such as hospitals, and implementing measures to control pigeon populations can significantly decrease the spread of pathogens.
