Ho Mcmahon (crowdpear3)
Fifty years ago, David Baltimore published a brief conceptual paper delineating the classification of viruses by the routes of genome expression. The six "Baltimore classes" of viruses, with a subsequently added 7th class, became the conceptual framework for the development of virology during the next five decades. During this time, it became clear that the Baltimore classes, with relatively minor additions, indeed cover the diversity of virus genome expression schemes that also define the replication cycles. Here, we examine the status of the Baltimore classes 50 years after their advent and explore their links with the global ecology and biology of the respective viruses. We discuss an extension of the Baltimore scheme and why many logically admissible expression-replication schemes do not appear to be realized in nature. Recent phylogenomic analyses allow tracing the complex connections between the Baltimore classes and the monophyletic realms of viruses. The five classes of RNA viruses and reverse-transcribing viruses share an origin, whereas both the single-stranded DNA viruses and double-stranded DNA (dsDNA) viruses evolved on multiple independent occasions. Most of the Baltimore classes of viruses probably emerged during the earliest era of life evolution, at the stage of the primordial pool of diverse replicators, and before the advent of modern-like cells with large dsDNA genomes. The Baltimore classes remain an integral part of the conceptual foundation of biology, providing the essential structure for the logical space of information transfer processes, which is nontrivially connected with the routes of evolution of viruses and other replicators. Autism spectrum disorder (ASD) is a major public health concern caused by complex genetic and environmental components. Mechanisms of gene-environment ( G × E ) interactions and reliable biomarkers associated with ASD are mostly unknown or controversial. Induced pluripotent stem cells (iPSCs) from patients or with clustered regularly interspaced short palindromic repeats and CRISPR-associated protein 9 (CRISPR/Cas9)-introduced mutations in candidate ASD genes provide an opportunity to study ( G × E ) interactions. In this study, we aimed to identify a potential synergy between mutation in the high-risk autism gene encoding chromodomain helicase DNA binding protein 8 ( ) and environmental exposure to an organophosphate pesticide (chlorpyrifos; CPF) in an iPSC-derived human three-dimensional (3D) brain model. This study employed human iPSC-derived 3D brain organoids (BrainSpheres) carrying a heterozygote CRISPR/Cas9 BrainSpheres to chemical insult establishes a possibly broader role of ( G × E ) interaction in ASD. https//doi.org/10.1289/EHP8580. This study pioneered (G×E) interaction in iPSC-derived organoids. The experimental strategy enables biomonitoring and environmental risk assessment for ASD. Our findings reflected some metabolic perturbations and disruption of neurotransmitter systems involved in ASD. The increased susceptibility of CHD8+/- BrainSpheres to chemical insult establishes a possibly broader role of (G×E) interaction in ASD. https//doi.org/10.1289/EHP8580.Emerging studies have highlighted the disproportionate role of Candida albicans in influencing both early community assembly of the bacterial microbiome and dysbiosis during allergic diseases and intestinal inflammation. Nonpathogenic colonization of the human gastrointestinal (GI) tract by C. albicans is common, and the role of this single fungal species in modulating bacterial community reassembly after broad-spectrum antibiotics can be readily r