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<jats:p>Disease and accompanying inflammation are uncommon outcomes of viral infection in humans. Clinical inflammation occurs if steady-state cell-intrinsic and leukocytic immunity to viruses fails. Inflammation attests to the attempts of newly recruited and activated leukocytes to resolve infection in the blood or tissues. In the confusing battle between a myriad of viruses and cells, studies of human genetics can separate the root cause of inflammation and disease from its consequences. Single-gene inborn errors of cell-intrinsic or leukocytic immunity underlying diverse infections in the skin, brain, or lungs can help to clarify the human determinants of viral disease. The genetic elucidation of immunological deficits in a single patient with a specific vulnerability profile can reveal mechanisms of inflammation and disease that may be triggered by other causes, inherited or otherwise, in other patients. This human genetic dissection of viral infections is giving rise to a new biology and a new medicine.</jats:p>

<jats:p>The brain and gastrointestinal tract are critical sensory organs responsible for detecting, relaying, integrating, and responding to signals derived from the internal and external environment. At the interface of this sensory function, immune cells in the intestines and brain consistently survey environmental factors, eliciting responses that inform on the physiological state of the body. Recent research reveals that cross-talk along the gut-brain axis regulates inflammatory nociception, inflammatory responses, and immune homeostasis. Here, we discuss molecular and cellular mechanisms involved in the signaling of inflammation across the gut-brain axis. We further highlight interactions between the gut and the brain in inflammation-associated diseases.</jats:p>

<jats:p> Highlights from the <jats:italic>Science</jats:italic> family of journals </jats:p>

<jats:p>Editors’ selections from the current scientific literature</jats:p>

<jats:title>A tool to study SARS-CoV-2</jats:title> <jats:p> Work with infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) requires high-level biocontainment facilities, making it important to develop safer molecular tools that can potentially be used under less stringent conditions. Self-replicating RNAs known as replicons have long been used to study pathogenic RNA viruses; however, developing replicons to study SARS-SoV-2 has been challenging because of its large genome. Ricardo-Lax <jats:italic>et al</jats:italic> . used a yeast-based system to construct SARS-CoV-2 replicons that cannot assemble infectious virus because they lack the spike protein required for host cell entry. Transfecting cells with a spike-expressing plasmid and separately with the replicon generates replicon delivery particles (RDPs) that are only capable of one cycle of infection. The replicons and the RDPs can be used in different contexts for drug screening, and viral assays. —VV </jats:p>

<jats:title>Disease and hippocampal dysfunction</jats:title> <jats:p> Impaired function of the brain’s hippocampus can underpin psychiatric symptoms and cognitive impairment. Looking at postmortem brain samples from patients affected by any of several neurodegenerative disorders, Terreros-Roncal <jats:italic>et al</jats:italic> . investigated whether adult neurogenesis was disrupted (see the Perspective by Gage). Indeed, functions of the neurogenic niche shifted and the cells produced were abnormal in shape and differentiation. The neuronal plasticity characteristic of the hippocampus may make it especially susceptible to the ravages of neurodegenerative disease. —PJH </jats:p>

<jats:title>Organized by unstructured motifs</jats:title> <jats:p> The high degree of conservation in protein sequences thought to be unstructured has hinted that these regions may have important biological functions. Although unstructured regions are widely viewed to be crucial for protein signaling, localization, and stability, their roles in many other settings have remained mysterious. Cermakova <jats:italic>et al</jats:italic> . discovered that prominent members of the transcription elongation machinery are linked through a network of interactions involving transcription elongation factor TFIIS N-terminal domains (TNDs) and conserved unstructured sequences called “TND-interacting motifs” (TIMs). The researchers found that mutation of a single TIM in a central organizing protein of this network abolished key protein interactions and induced widespread defects in transcription elongation dynamics. —DJ </jats:p>

<jats:title>Quantum nature of roaming dynamics</jats:title> <jats:p> Despite intense study, roaming systems have been generally treated classically and their dynamics have been assumed to be ergodic. Foley <jats:italic>et al</jats:italic> . provide a combined experimental and theoretical study of the photodissociation of formaldehyde near the threshold for radical production. Their observations revealed a strong dependence of the degree of roaming on the rotational state of the molecule that is excited, which is indicative of an important role for quantum orbiting resonances. This study demonstrates unexpected, non-ergodic roaming dynamics in the prototypical roaming system that does not fit into the conventional classical picture, subject to further studies in other systems. —YS </jats:p>

<jats:title>Ancestry shapes genetic immune responses</jats:title> <jats:p> Selection for genes affecting the immune system can vary among populations because of selection for local environments. In humans, ancestry has been associated with different responses to infection. Randolph <jats:italic>et al</jats:italic> . examined the molecular determinants of these observations using single-cell RNA sequencing of immune cells from individuals of European and African descent who were infected with influenza in vitro. The experiments showed that infection-induced gene signatures diverged in a cell-type-specific manner that was correlated with ancestry, and that these observed ancestry-related differences were caused by changes in gene regulation and processes involved in transcription and translation. —LMZ </jats:p>

<jats:title>Learning to stabilize palladium dimers</jats:title> <jats:p> Catalyst optimization is often difficult to do rationally. Once something works, it may be unclear which specific features underpin the performance. A case in point is the stabilization of palladium(I) dimers, which has relied on a very small class of phosphine ligands. Hueffel <jats:italic>et al</jats:italic> . used machine learning to search for patterns in this known class of ligands and thereby guide the discovery of variants that likewise stabilize the dimers. The authors were able to synthesize eight previously unreported dimers. —JSY </jats:p>