Catálogo de publicaciones - revistas

<jats:title>Promising antiviral protease inhibitors</jats:title> <jats:p> With no vaccine or proven effective drug against the virus that causes coronavirus disease 2019 (COVID-19), scientists are racing to find clinical antiviral treatments. A promising drug target is the viral main protease M <jats:sup>pro</jats:sup> , which plays a key role in viral replication and transcription. Dai <jats:italic>et al.</jats:italic> designed two inhibitors, 11a and 11b, based on analyzing the structure of the M <jats:sup>pro</jats:sup> active site. Both strongly inhibited the activity of M <jats:sup>pro</jats:sup> and showed good antiviral activity in cell culture. Compound 11a had better pharmacokinetic properties and low toxicity when tested in mice and dogs, suggesting that this compound is a promising drug candidate. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1331" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abb4489">1331</jats:related-article> </jats:p>

<jats:title>Resistance to influenza antibodies</jats:title> <jats:p> Broadly neutralizing human antibodies (bnAbs) to the stem of hemagglutinin (HA), a trimeric glycoprotein found on the surface of influenza viruses, are valuable therapeutics and can guide the development of universal influenza vaccines. For their use in therapy development, it is important to understand the extent to which HA stem variants with resistance to bnAbs can develop. Wu <jats:italic>et al.</jats:italic> used saturation mutagenesis combined with next-generation sequencing to systematically search for resistance mutations to prototypic bnAbs in two influenza subtypes, H3 and H1. They found that the genetic barrier to resistance to stem bnAbs was low for the H3 subtype but higher for the H1 subtype. The ability of H3 to develop resistance to bnAbs presents a challenge in the development of a universal influenza vaccine. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1335" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.aaz5143">1335</jats:related-article> </jats:p>

<jats:p>Global biodiversity assessments have highlighted land-use change as a key driver of biodiversity change. However, there is little empirical evidence of how habitat transformations such as forest loss and gain are reshaping biodiversity over time. We quantified how change in forest cover has influenced temporal shifts in populations and ecological assemblages from 6090 globally distributed time series across six taxonomic groups. We found that local-scale increases and decreases in abundance, species richness, and temporal species replacement (turnover) were intensified by as much as 48% after forest loss. Temporal lags in population- and assemblage-level shifts after forest loss extended up to 50 years and increased with species’ generation time. Our findings that forest loss catalyzes population and biodiversity change emphasize the complex biotic consequences of land-use change.</jats:p>

<jats:title>Strong and tough steel</jats:title> <jats:p> Ultrahard materials often do not have similarly impressive fracture toughness. Liu <jats:italic>et al.</jats:italic> discovered a processing route for medium manganese steel alloy in which ultrahigh strength accompanies high fracture toughness. The steel relies on both transformation-induced plasticity and delamination toughening to boost the fracture properties. The steel is composed of less expensive elements, making it a potentially inexpensive material attractive for structural applications. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1347" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.aba9413">1347</jats:related-article> </jats:p>

<jats:title>Cutting it close for radical coupling</jats:title> <jats:p> In principle, electrochemistry is an ideal method for radical coupling: One precursor oxidized at the anode pairs up with a counterpart that has been reduced at the cathode. The trouble is that either or both coupling partners might not stay stable long enough to meet in the middle. Mo <jats:italic>et al.</jats:italic> resolved this issue by closely spacing the electrodes in a microfluidics platform (see the Perspective by Liu <jats:italic>et al.</jats:italic> ). They showcase coupling of dicyanobenzene as the cathodic radical precursor with a variety of oxidatively generated partners. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1352" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.aba3823">1352</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1312" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abc2985">1312</jats:related-article> </jats:p>

<jats:title>Seismic swarms show the structure</jats:title> <jats:p> Faults responsible for earthquakes are idealized into two dimensions, despite fault zones being complicated, three-dimensional structures. Ross <jats:italic>et al.</jats:italic> used machine learning to find 22,000 seismic events near Cahuilla, California, during a seismic swarm. They used the locations and sizes of these events to show how the complex structure of the fault interacted with natural fluid injections from below. The authors' methods highlight the complexities of one fault and suggest a way to characterize other faults around the world. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1357" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abb0779">1357</jats:related-article> </jats:p>

<jats:title>Mobile symptom tracking</jats:title> <jats:p> The rapidity with which severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads through a population is defying attempts at tracking it, and quantitative polymerase chain reaction testing so far has been too slow for real-time epidemiology. Taking advantage of existing longitudinal health care and research patient cohorts, Drew <jats:italic>et al.</jats:italic> pushed software updates to participants to encourage reporting of potential coronavirus disease 2019 (COVID-19) symptoms. The authors recruited about 2 million users (including health care workers) to the COVID Symptom Study (previously known as the COVID Symptom Tracker) from across the United Kingdom and the United States. The prevalence of combinations of symptoms (three or more), including fatigue and cough, followed by diarrhea, fever, and/or anosmia, was predictive of a positive test verification for SARS-CoV-2. As exemplified by data from Wales, United Kingdom, mathematical modeling predicted geographical hotspots of incidence 5 to 7 days in advance of official public health reports. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1362" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abc0473">1362</jats:related-article> </jats:p>

<jats:title>Older origins of measles virus</jats:title> <jats:p> Animal domestication by humans is thought to have given many pathogens an opportunity to invade a new host, and measles is one example of this. However, there is controversy about when measles emerged in humans, because the historical descriptions of measles are relatively recent (late ninth century CE). The controversy has persisted in part because ancient RNA is thought to be a poor target for molecular clock techniques. Düx <jats:italic>et al.</jats:italic> have overcome the ancient RNA challenge by sequencing a measles virus genome obtained from a museum specimen of the lungs of child who died in 1912 (see the Perspective by Ho and Duchêne). The authors used these and other more recent sequencing data in a Bayesian molecular clock–modeling technique, which showed that measles virus diverged from rinderpest virus in the sixth century BCE, indicating an early origin for measles possibly associated with the beginnings of urbanization. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1367" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.aba9411">1367</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1310" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.abc5746">1310</jats:related-article> </jats:p>

<jats:title>Inflammaging? Blame T cells!</jats:title> <jats:p> Mitochondrial dysfunction in various tissues is a prominent characteristic of age-related deterioration, but it is unclear how mitochondrial dysfunction in particular cell types contributes to this process. Desdín-Micó <jats:italic>et al.</jats:italic> generated mice with T cells that were specifically deficient in a mitochondrial DNA–stabilizing protein. These animals exhibited multiple features associated with aging, including neurological, metabolic, muscular, and cardiovascular impairments. The defective T cells initiated an inflammatory program similar to that observed in older animals, a process called “inflammaging.” Blocking the cytokine tumor necrosis factor–α or administering precursors of the cofactor nicotinamide adenine dinucleotide restored many of these symptoms of senescence. These findings may potentially inform future therapies for age-associated diseases, as well as cachexia and cytokine-release syndrome. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6497" page="1371" related-article-type="in-this-issue" vol="368" xlink:href="10.1126/science.aax0860">1371</jats:related-article> </jats:p>