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Viral afterlife: SARS-CoV-2 as a reservoir of immunomimetic peptides that reassemble into proinflammatory supramolecular complexes | PNAS
▻https://www.pnas.org/doi/abs/10.1073/pnas.2300644120
▻https://www.pnas.org/cms/asset/e2e81613-f4a7-4700-ab95-679bd0354e48/keyimage.jpg
Existence of exogenous mimics of pro-inflammatory host antimicrobial peptides (xenoAMPs) in SARS-CoV-2 proteins. (A) SARS-CoV-2 proteins are scanned with a machine learning AMP classifier. Each queried sequence is given a σ score that measures its AMP-ness. Three representative high-scoring sequences are studied: xenoAMP(ORF1ab), xenoAMP(S) and xenoAMP(M). The grey bars mark the location where the corresponding sequences are selected. (B) SARS-CoV-2 sequences are aligned and compared to their homologs in a common cold human coronavirus HCoV-OC43: Control (ORF1ab), Control(S) and Control(M). Asterisks, colons, and periods indicate positions that have fully conserved residues, those that have strongly similar properties, and those that have weakly similar properties, respectively. Color is assigned to each residue using the ClustalX scheme. (C) σ score heatmaps compare the distribution of high scoring sequences in three proteins from SARS-CoV-2 and HCoV-OC43. The first amino acid in each sequence is colored according to its average σ score; regions with negative average σ scores (non-AMPs) are colored white. “Hot spot” clusters of high-scoring sequences for SARS-CoV-2 (bright yellow regions bracketed in red boxes) have systematically higher scores and span wider regions of sequence space compared to HCoV-OC43. This trend suggests that hot spots in SARS-CoV-2 can generate higher scoring sequences for a greater diversity of enzymatic cleavage sites than those in HCoV-OC43.

Significance
At present, there are no criteria to evaluate whether a coronavirus can cause pandemics with severe inflammation or just common colds. We provide a possible answer by considering the virus not only as an infectious agent but as a reservoir of replicated peptide motifs that are not themselves pathogen associated molecular patterns (PAMPs) that specifically bind to pattern recognition receptors but are nevertheless capable of drastic immune amplification via self-assembly with PAMPs. We show evidence that viral peptide fragments from SARS-CoV-2 but not harmless coronavirus homologs can “reassemble” with dsRNA into a form of proinflammatory nanocrystalline condensed matter, resulting in cooperative, multivalent immune recognition and grossly amplified inflammatory responses.

Abstract
It is unclear how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leads to the strong but ineffective inflammatory response that characterizes severe Coronavirus disease 2019 (COVID-19), with amplified immune activation in diverse cell types, including cells without angiotensin-converting enzyme 2 receptors necessary for infection. Proteolytic degradation of SARS-CoV-2 virions is a milestone in host viral clearance, but the impact of remnant viral peptide fragments from high viral loads is not known. Here, we examine the inflammatory capacity of fragmented viral components from the perspective of supramolecular self-organization in the infected host environment. Interestingly, a machine learning analysis to SARS-CoV-2 proteome reveals sequence motifs that mimic host antimicrobial peptides (xenoAMPs), especially highly cationic human cathelicidin LL-37 capable of augmenting inflammation. Such xenoAMPs are strongly enriched in SARS-CoV-2 relative to low-pathogenicity coronaviruses. Moreover, xenoAMPs from SARS-CoV-2 but not low-pathogenicity homologs assemble double-stranded RNA (dsRNA) into nanocrystalline complexes with lattice constants commensurate with the steric size of Toll-like receptor (TLR)-3 and therefore capable of multivalent binding. Such complexes amplify cytokine secretion in diverse uninfected cell types in culture (epithelial cells, endothelial cells, keratinocytes, monocytes, and macrophages), similar to cathelicidin’s role in rheumatoid arthritis and lupus. The induced transcriptome matches well with the global gene expression pattern in COVID-19, despite using <0.3% of the viral proteome. Delivery of these complexes to uninfected mice boosts plasma interleukin-6 and CXCL1 levels as observed in COVID-19 patients.

Bringing a physicist’s mindset to the biosciences | UCLA
22/07/2022
▻https://newsroom.ucla.edu/stories/gerard-wong-brings-physicist-mindset-biosciences

https://s3.amazonaws.com/cms.ipressroom.com/173/files/20226/62d9b44e2cfac22252a56a6b_Gerard+Wong/Gerard%20Wong_mid.jpg

UCLA’s Gerard Wong approaches life sciences with an eye for connection and a distrust of metaphors
In his lab, Gerard Wong, professor of bioengineering at the UCLA Samueli School of Engineering, explores the molecular mechanisms behind basic processes of life and their influence on human health. But his original training was far afield — in physics, working with solids and liquids at the smallest scales.

That shift in scientific focus isn’t unprecedented, but the way Wong bridges the disparate disciplines is unusual. By applying not only instrumentation but also ideas from physics to biology, he has uncovered surprising links between the fields, which could have implications for bioscience and disease treatment.
[…]
For instance, one part of his current research program focuses on autoimmune diseases, which are typically viewed as a malfunction in a coordinated defense system. He aims to reveal how inflammation works at a more fundamental level, as a system that obeys physical laws.

“We imagine that the immune system recognizes something in a similar way to how we recognize something: This is DNA, this is RNA, this other thing is a part of the bacterial flagellum,” Wong said. “Nature might instead work through geometric shapes and sizes, entropy, interaction or lack of interaction with water, interactions between charged particles — in terms of the excruciatingly low-level, detailed, unifying language of physics.”

Taking this approach, the researchers revealed how certain molecules amp up the immune response, which can have applications to lupus, psoriasis, arthritis and other diseases.

Farmland practices are driving bird population decline across Europe | PNAS
▻https://www.pnas.org/doi/10.1073/pnas.2216573120

https://www.pnas.org/cms/asset/0d1ae1e2-4300-4bbb-b0c4-497149688d0f/keyimage.jpg

Significance
Using the most recent and largest empirical dataset ever assembled for Europe to investigate the effect of anthropogenic pressures, we highlighted the predominant detrimental impact of agriculture intensification on avian biodiversity at a continental scale over climate change, urbanization, and forest cover changes. Our results do not simply quantify correlations, but our analytical design is meant to strive for more quasicausal responses of bird populations to global change drivers. This paper contributes to the highest political and technical challenge faced by agricultural policy in Europe, struggling to balance high productivity from intensive agricultural practices with environmental protection, and the results are therefore crucial to policymakers, scientists, and the general public concerned for biodiversity and global change issues.

Abstract
Declines in European bird populations are reported for decades but the direct effect of major anthropogenic pressures on such declines remains unquantified. Causal relationships between pressures and bird population responses are difficult to identify as pressures interact at different spatial scales and responses vary among species. Here, we uncover direct relationships between population time-series of 170 common bird species, monitored at more than 20,000 sites in 28 European countries, over 37 y, and four widespread anthropogenic pressures: agricultural intensification, change in forest cover, urbanisation and temperature change over the last decades. We quantify the influence of each pressure on population time-series and its importance relative to other pressures, and we identify traits of most affected species. We find that agricultural intensification, in particular pesticides and fertiliser use, is the main pressure for most bird population declines, especially for invertebrate feeders. Responses to changes in forest cover, urbanisation and temperature are more species-specific. Specifically, forest cover is associated with a positive effect and growing urbanisation with a negative effect on population dynamics, while temperature change has an effect on the dynamics of a large number of bird populations, the magnitude and direction of which depend on species’ thermal preferences. Our results not only confirm the pervasive and strong effects of anthropogenic pressures on common breeding birds, but quantify the relative strength of these effects stressing the urgent need for transformative changes in the way of inhabiting the world in European countries, if bird populations shall have a chance of recovering.

Alors la disparition des oiseaux, c’est comme pour le réchauffement climatique. C’est un complot wokiste pour empêcher les paysans de travailler et de nourrir la planète. Personne ne parle de la matière noire qui réchauffe la galaxie et qui est à l’origine du réchauffement actuel ? Pourquoi ? Qui en profite ? Les écoterroristes pardi ! Et c’est pareil pour les oiseaux. S’ils disparaissent, ce qui reste à prouver, c’est à priori parce que la matière noire de l’univers n’aime pas les oiseaux, et que les oiseaux préfèrent se cacher. En conséquence, les écoterroristes ne peuvent plus compter les oiseaux, et on finit par croire qu’ils ont disparus à cause des paysans ukrainiens qui nourrissent les habitants du Sahel et du Biafra et qu’on voudrait empêcher de travailler pour de mauvaises raisons.

(désolé)

Ça fait 50 ans maintenant qu’il est scientifiquement « urgent de… » et que chaque année il y a une nouvelle étude majeure, avec des chiffres et des graphiques et des projections, qui conclue que non vraiment là ce n’est plus possible, et qu’il est encore plus urgent de…

Et rien.

La folie, c’est de faire toujours la même chose et de s’attendre à un résultat différent.
– comme dirait l’autre

Du coup la méthode scientifique, même produisant des choses vraies, est-elle vraiment la bonne solution ? Ya de quoi légitimement se poser la question, après 50 ans d’échecs évidents (le monde est bien bien pire et bien bien plus détruit qu’en 1972).

Preuve en est seulement que les sciences et leurs progrès ne sont pas indépendants des rapports sociaux de production dans lesquels ils prennent place. Dans une société dont l’économie obéit aux seules logiques de la recherche de profit, les sciences ne seront jamais une solution.

▻https://seenthis.net/messages/1003093
▻https://seenthis.net/messages/1003089

#écologie #oiseaux #pollution

Un centre d’étude de l’UQAM (université du Québec à Montréal) fait paraître une revue sur le thème de l’éducation relative à l’environnement (ERE). Dans une de ses productions (volume 17-1 de 2022), les auteurs passent au crible les problématiques qui impactent les actions contre le changement climatique et contre la dégradation de l’environnement en général. Abordé sous l’angle de la psycho-sociologie, cette analyse tente de répondre aux questions posées par l’inaction (on le sait pourtant depuis longtemps, mais on ne fait toujours rien).
Plan de l’exposé :

-Sciences cognitives et changements climatiques
–Défi de la compréhension
–Le défi de l’action climatique
–Le défi du déni climatique
–Limites méthodologiques et épistémologiques de certaines approches psychologiques
–La crise de reproductibilité associée aux approches expérimentales
–Validité externe
–Déterminisme de l’inaction et du déni
–Limites des explications individualistes
–Limites politiques
–Pathologisation du déni
–« Nudging » et marketing social
–Post-démocratie
–Discussion
–Conclusion

Le lien : ▻https://journals.openedition.org/ere/8307

(Pas encore pris le temps de tout lire mais ça a l’air honnête)